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Journal articles on the topic 'FOXP4'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Li, Shanru, Joel Weidenfeld, and Edward E. Morrisey. "Transcriptional and DNA Binding Activity of the Foxp1/2/4 Family Is Modulated by Heterotypic and Homotypic Protein Interactions." Molecular and Cellular Biology 24, no. 2 (January 15, 2004): 809–22. http://dx.doi.org/10.1128/mcb.24.2.809-822.2004.

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ABSTRACT Foxp1, Foxp2, and Foxp4 are large multidomain transcriptional regulators belonging to the family of winged-helix DNA binding proteins known as the Fox family. Foxp1 and Foxp2 have been shown to act as transcriptional repressors, while regulatory activity of the recently identified Foxp4 has not been determined. Given the importance of this Fox gene subfamily in neural and lung development, we sought to elucidate the mechanisms by which Foxp1, Foxp2, and Foxp4 repress gene transcription. We show that like Foxp1 and Foxp2, Foxp4 represses transcription. Analysis of the N-terminal repression domain in Foxp1, Foxp2, and Foxp4 shows that this region contains two separate and distinct repression subdomains that are highly homologous termed subdomain 1 and subdomain 2. However, subdomain 2 is not functional in Foxp4. Screening for proteins that interact with subdomains 1 and 2 of Foxp2 using yeast two-hybrid analysis revealed that subdomain 2 binds to C-terminal binding protein 1, which can synergistically repress transcription with Foxp1 and Foxp2, but not Foxp4. Subdomain 1 contains a highly conserved leucine zipper similar to that found in N-myc and confers homo- and heterodimerization to the Foxp1/2/4 family members. These interactions are dependent on the conserved leucine zipper motif. Finally, we show that the integrity of this subdomain is essential for DNA binding, making Foxp1, Foxp2, and Foxp4 the first Fox proteins that require dimerization for DNA binding. These data reveal a complex regulatory mechanism underlying Foxp1, Foxp2, and Foxp4 activity, demonstrating that Foxp1, Foxp2, and Foxp4 are the first Fox proteins reported whose activity is regulated by homo- and heterodimerization.

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2

Sin, Cora, Hongyan Li, and Dorota A. Crawford. "Transcriptional Regulation by FOXP1, FOXP2, and FOXP4 Dimerization." Journal of Molecular Neuroscience 55, no. 2 (July 16, 2014): 437–48. http://dx.doi.org/10.1007/s12031-014-0359-7.

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3

Mendoza, Ezequiel, Kirill Tokarev, Daniel N. Düring, Eva Camarillo Retamosa, Michael Weiss, Nshdejan Arpenik, and Constance Scharff. "Differential coexpression of FoxP1, FoxP2, and FoxP4 in the Zebra Finch (Taeniopygia guttata) song system." Journal of Comparative Neurology 523, no. 9 (April 2, 2015): 1318–40. http://dx.doi.org/10.1002/cne.23731.

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4

Liang, Jingchen, Duo Wang, Guanhua Qiu, Xiaoqi Zhu, Junjie Liu, Hang Li, and Pingping Guo. "Long Noncoding RNA FOXP4-AS1 Predicts Unfavourable Prognosis and Regulates Proliferation and Invasion in Hepatocellular Carcinoma." BioMed Research International 2021 (February 1, 2021): 1–12. http://dx.doi.org/10.1155/2021/8850656.

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Background. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer that has a high level of morbidity and mortality. Long noncoding RNA (lncRNA) is a novel regulatory factor of tumour proliferation, apoptosis, and metastasis. Our previous studies indicated that lncRNA FOXP4-AS1 is a functional oncogene in HCC; thus, this study is aimed at further evaluating the clinical and biological function of FOXP4-AS1 in HCC. Material and Methods. First, we detected the expression of FOXP4-AS1 in HCC tissues and paracarcinoma normal tissues by qRT-PCR. Second, the prognostic effects of FOXP4-AS1 in patients with HCC were analysed in a training group and a verification group. Subsequently, to investigate the biological effects of FOXP4-AS1 on HCC cells, downexpression tests were further conducted. Results. The expression of FOXP4-AS1 was higher in HCC tissues than adjacent nontumourous tissues, whereas the low expression of FOXP4-AS1 was correlated with optimistic treatment outcomes, which suggested that FOXP4-AS1 may be an independent prognostic biomarker for HCC. Moreover, the downregulation of FOXP4-AS1 significantly reduced the cell proliferation and clonal abilities and inhibited the invasion, migration, and angiogenesis of hepatoma cells ( P < 0.05 ). Conclusion. These results revealed the clinical significance and biological function of FOXP4-AS1 in HCC development, which may provide a new direction for finding therapeutic targets and potential prognostic biomarkers of HCC.

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5

Bowers, J. Michael, and Genevieve Konopka. "The Role of the FOXP Family of Transcription Factors in ASD." Disease Markers 33, no. 5 (2012): 251–60. http://dx.doi.org/10.1155/2012/456787.

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Autism spectrum disorders (ASD) is a neurodevelopmental disease with complex genetics; however, the genes that are responsible for this disease still remain mostly unknown. Here, we focus on the FOXP family of transcription factors as there is emerging evidence strongly linking these genes to ASD and other genes implicated in ASD. The FOXP family of genes includes three genes expressed in the central nervous system: FOXP1, FOPX2, and FOXP4. This unique group of transcription factors has known functions in brain development as well as the evolution of language. We will also discuss the other genes including transcriptional targets of FOXP genes that have been found to be associated with language and may be important in the pathophysiology of ASD. Finally, we will review the emerging animal models currently being used to study the function of the FOXP genes within the context of ASD symptomology. The combination of gene expression and animal behavior is critical for elucidating how genes such as the FOXP family members are key players within the framework of the developing brain.

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6

Lu, Min Min, Shanru Li, Honghua Yang, and Edward E. Morrisey. "Foxp4: a novel member of the Foxp subfamily of winged-helix genes co-expressed with Foxp1 and Foxp2 in pulmonary and gut tissues." Mechanisms of Development 119 (December 2002): S197—S202. http://dx.doi.org/10.1016/s0925-4773(03)00116-3.

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7

Lu, Min Min, Shanru Li, Honghua Yang, and Edward E. Morrisey. "RETRACTED: Foxp4: a novel member of the Foxp subfamily of winged-helix genes co-expressed with Foxp1 and Foxp2 in pulmonary and gut tissues." Gene Expression Patterns 2, no. 3-4 (December 2002): 223–28. http://dx.doi.org/10.1016/s1567-133x(02)00058-3.

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8

Spaeth, Jason M., Chad S. Hunter, Lauren Bonatakis, Min Guo, Catherine A. French, Ian Slack, Manami Hara, et al. "The FOXP1, FOXP2 and FOXP4 transcription factors are required for islet alpha cell proliferation and function in mice." Diabetologia 58, no. 8 (May 29, 2015): 1836–44. http://dx.doi.org/10.1007/s00125-015-3635-3.

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9

Norton, Philipp, Peggy Barschke, Constance Scharff, and Ezequiel Mendoza. "Differential Song Deficits after Lentivirus-Mediated Knockdown of FoxP1, FoxP2, or FoxP4 in Area X of Juvenile Zebra Finches." Journal of Neuroscience 39, no. 49 (October 22, 2019): 9782–96. http://dx.doi.org/10.1523/jneurosci.1250-19.2019.

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10

Teufel, Andreas, Eric A. Wong, Mahua Mukhopadhyay, Nasir Malik, and Heiner Westphal. "FoxP4, a novel forkhead transcription factor." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1627, no. 2-3 (June 2003): 147–52. http://dx.doi.org/10.1016/s0167-4781(03)00074-5.

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11

Li, Yonghui, Tingting Li, Yongbin Yang, Wenli Kang, Shaoyong Dong, and Shujie Cheng. "YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of esophageal squamous cell carcinoma cells." Cell Biology International 44, no. 7 (April 20, 2020): 1447–57. http://dx.doi.org/10.1002/cbin.11338.

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12

Perie, Luce, Narendra Verma, and Elisabetta Mueller. "The forkhead box transcription factor FoxP4 regulates thermogenic programs in adipocytes." Journal of Lipid Research 62 (2021): 100102. http://dx.doi.org/10.1016/j.jlr.2021.100102.

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13

Park, Yongkyu, Midori Lofton, Diana Li, and Mladen-Roko Rasin. "Extrinsic Regulators of mRNA Translation in Developing Brain: Story of WNTs." Cells 10, no. 2 (January 28, 2021): 253. http://dx.doi.org/10.3390/cells10020253.

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Extrinsic molecules such as morphogens can regulate timed mRNA translation events in developing neurons. In particular, Wingless-type MMTV integration site family, member 3 (Wnt3), was shown to regulate the translation of Foxp2 mRNA encoding a Forkhead transcription factor P2 in the neocortex. However, the Wnt receptor that possibly mediates these translation events remains unknown. Here, we report Frizzled member 7 (Fzd7) as the Wnt3 receptor that lays downstream in Wnt3-regulated mRNA translation. Fzd7 proteins co-localize with Wnt3 ligands in developing neocortices. In addition, the Fzd7 proteins overlap in layer-specific neuronal subpopulations expressing different transcription factors, Foxp1 and Foxp2. When Fzd7 was silenced, we found decreased Foxp2 protein expression and increased Foxp1 protein expression, respectively. The Fzd7 silencing also disrupted the migration of neocortical glutamatergic neurons. In contrast, Fzd7 overexpression reversed the pattern of migratory defects and Foxp protein expression that we found in the Fzd7 silencing. We further discovered that Fzd7 is required for Wnt3-induced Foxp2 mRNA translation. Surprisingly, we also determined that the Fzd7 suppression of Foxp1 protein expression is not Wnt3 dependent. In conclusion, it is exhibited that the interaction between Wnt3 and Fzd7 regulates neuronal identity and the Fzd7 receptor functions as a downstream factor in ligand Wnt3 signaling for mRNA translation. In particular, the Wnt3-Fzd7 signaling axis determines the deep layer Foxp2-expressing neurons of developing neocortices. Our findings also suggest that Fzd7 controls the balance of the expression for Foxp transcription factors in developing neocortical neurons. These discoveries are presented in our manuscript within a larger framework of this review on the role of extrinsic factors in regulating mRNA translation.

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14

Bowers, J. Michael, Miguel Perez-Pouchoulen, Clinton R. Roby, Timothy E. Ryan, and Margaret M. McCarthy. "Androgen Modulation of Foxp1 and Foxp2 in the Developing Rat Brain: Impact on Sex Specific Vocalization." Endocrinology 155, no. 12 (December 1, 2014): 4881–94. http://dx.doi.org/10.1210/en.2014-1486.

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Sex differences in vocal communication are prevalent in both the animals and humans. The mechanism(s) mediating gender differences in human language are unknown, although, sex hormones, principally androgens, play a central role in the development of vocalizations in a wide variety of animal species. The discovery of FOXP2 has added an additional avenue for exploring the origins of language and animal communication. The FOXP2 gene is a member of the forkhead box P (FOXP) family of transcription factors. Prior to the prenatal androgen surge in male fetuses, we observed no sex difference for Foxp2 protein levels in cultured cells. In contrast, 24 hours after the onset of the androgen surge, we found a sex difference for Foxp2 protein levels in cultured cortical cells with males having higher levels than females. Furthermore, we observed the potent nonaromatizable androgen dihydrotestosterone altered not only Foxp2 mRNA and protein levels but also Foxp1. Androgen effects on both Foxp2 and Foxp1 were found to occur in the striatum, cerebellar vermis, and cortex. Immunofluorescence microscopy and coimmunoprecipitation demonstrate Foxp2 and the androgen receptor protein interact. Databases for transcription factor binding sites predict a consensus binding motif for androgen receptor on the Foxp2 promoter regions. We also observed a sex difference in rat pup vocalization with males vocalizing more than females and treatment of females with dihydrotestosterone eliminated the sex difference. We propose that androgens might be an upstream regulator of both Foxp2 and Foxp1 expression and signaling. This has important implications for language and communication as well as neuropsychiatric developmental disorders involving impairments in communication.

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15

Ma, Tao, and Jin Zhang. "Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT." Cancer Management and Research Volume 11 (April 2019): 2783–93. http://dx.doi.org/10.2147/cmar.s191641.

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16

Wiehagen, Karla R., Evann Corbo-Rodgers, Shanru Li, Elizabeth S. Staub, Christopher A. Hunter, Edward E. Morrisey, and Jonathan S. Maltzman. "Foxp4 Is Dispensable for T Cell Development, but Required for Robust Recall Responses." PLoS ONE 7, no. 8 (August 13, 2012): e42273. http://dx.doi.org/10.1371/journal.pone.0042273.

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17

Tam, W. Y., C. K. Y. Leung, K. K. Tong, and K. M. Kwan. "Foxp4 is essential in maintenance of purkinje cell dendritic arborization in the mouse cerebellum." Neuroscience 172 (January 2011): 562–71. http://dx.doi.org/10.1016/j.neuroscience.2010.10.023.

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18

Shirshev, S. V., I. V. Nekrasova, O. L. Gorbunova, and E. G. Orlova. "Regulation of recombinase RAG-1 expression by female sex steroids in Treg and Th17 lymphocytes. role of oncostatin M." Доклады Академии наук 484, no. 5 (May 16, 2019): 641–44. http://dx.doi.org/10.31857/s0869-56524845641-644.

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The effect of estradiol (E2), progesterone (P4), and oncostatin M (OSM) on the differentiation of CD4+ T cells to T regulatory (Treg) lymphocytes and T helpers 17 (Th17) was investigated. The possibility of revision of the T cell receptor in these subpopulations by evaluating the expression of RAG-1 recombinase was also studied. E2 at concentrations characteristic of pregnancy trimester I, but no P4 or OSM, increased the Treg level. Combination of sex steroids with OSM increased the percent of CD4+FOXP4+ cells and enhanced RAG-1 expression in these cells, thus promoting the development of immune tolerance during pregnancy. In the study of Th17 such effect of the hormones and OSM was not detected.

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19

Wang, Duo, Tao Bai, Guanyu Chen, Junjie Liu, Miao Chen, Yuan Zhao, Tao Luo, et al. "Upregulation of long non-coding RNA FOXP4-AS1 and its regulatory network in hepatocellular carcinoma." OncoTargets and Therapy Volume 12 (August 2019): 7025–38. http://dx.doi.org/10.2147/ott.s220923.

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20

Xu, Yaoxiang, Yanshan Liu, Wenlin Xiao, Jin Yue, Lingfa Xue, Qunli Guan, Jing Deng, and Jian Sun. "MicroRNA-299-3p/FOXP4 Axis Regulates the Proliferation and Migration of Oral Squamous Cell Carcinoma." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381987480. http://dx.doi.org/10.1177/1533033819874803.

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MicroRNAs are noncoding RNAs of 21 to 23 nucleotides in length that play important roles in almost all biological pathways. The roles of microRNA-299-3p in the development and progression of oral squamous cell carcinoma remain unclear. Expression level of microRNA-299-3p in oral squamous cell carcinoma cell lines was analyzed. Then, the effects of microRNA-299-3p on oral squamous cell carcinoma cell proliferation and migration were investigated. Moreover, bioinformation algorithm and Western blot were conducted to explore whether forkhead box P4 was a direct target of miR-299-3p. We showed that microRNA-299-3p expression was significantly reduced in oral squamous cell carcinoma cell lines. Next, overexpression of microRNA-299-3p was found to inhibit oral squamous cell carcinoma cell proliferation and migration but promote apoptosis. In addition, forkhead box P4 was identified as a functional target of microRNA-299-3p. Our results provide a new perspective for the mechanisms underlying the progression of oral squamous cell carcinoma and a novel target for the treatment of oral squamous cell carcinoma.

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21

Zhao, Juan, Ting Yang, and Long Li. "LncRNA FOXP4-AS1 Is Involved in Cervical Cancer Progression via Regulating miR-136-5p/CBX4 Axis." OncoTargets and Therapy Volume 13 (March 2020): 2347–55. http://dx.doi.org/10.2147/ott.s241818.

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22

E, Changyong, Jinghui Yang, Hang Li, and Chunsheng Li. "LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling." Cancer Management and Research Volume 11 (April 2019): 2871–79. http://dx.doi.org/10.2147/cmar.s197979.

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23

Wang, Xiaoli, Liming Liu, Wenfei Zhao, Qingyan Li, Guangsheng Wang, and Huahui Li. "LncRNA SNHG16 Promotes the Progression of Laryngeal Squamous Cell Carcinoma by Mediating miR-877-5p/FOXP4 Axis." OncoTargets and Therapy Volume 13 (May 2020): 4569–79. http://dx.doi.org/10.2147/ott.s250752.

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24

Huang, Changkun, Huanghao Deng, Yinhuai Wang, Hongyi Jiang, Ran Xu, Xuan Zhu, Zhichao Huang, and Xiaokun Zhao. "Circular RNA circABCC4 as the ceRNA of miR‐1182 facilitates prostate cancer progression by promoting FOXP4 expression." Journal of Cellular and Molecular Medicine 23, no. 9 (July 3, 2019): 6112–19. http://dx.doi.org/10.1111/jcmm.14477.

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25

Yang, Tian, Hong Li, Asmitananda Thakur, Tianjun Chen, Jing Xue, Dan Li, and Mingwei Chen. "FOXP4 modulates tumor growth and independently associates with miR-138 in non-small cell lung cancer cells." Tumor Biology 36, no. 10 (May 21, 2015): 8185–91. http://dx.doi.org/10.1007/s13277-015-3498-8.

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26

E, Changyong, Jinghui Yang, Hang Li, and Chunsheng Li. "LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling [Corrigendum]." Cancer Management and Research Volume 11 (May 2019): 3971–72. http://dx.doi.org/10.2147/cmar.s212734.

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27

Wang, Nan, Yuanting Gu, Lin Li, Fang Wang, Pengwei Lv, Youyi Xiong, and Xinguang Qiu. "Circular RNA circMYO9B facilitates breast cancer cell proliferation and invasiveness via upregulating FOXP4 expression by sponging miR-4316." Archives of Biochemistry and Biophysics 653 (September 2018): 63–70. http://dx.doi.org/10.1016/j.abb.2018.04.017.

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28

Li, Juan, Yifan Lian, Changsheng Yan, Zeling Cai, Jie Ding, Zhonghua Ma, Peng Peng, and Keming Wang. "Long non-coding RNA FOXP4-AS1 is an unfavourable prognostic factor and regulates proliferation and apoptosis in colorectal cancer." Cell Proliferation 50, no. 1 (October 27, 2016): e12312. http://dx.doi.org/10.1111/cpr.12312.

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29

Yang, Lei, Dawei Ge, Xi Chen, Junjun Qiu, Zhaowei Yin, Shengnai Zheng, and Chunzhi Jiang. "FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2." Biochemical and Biophysical Research Communications 502, no. 4 (August 2018): 493–500. http://dx.doi.org/10.1016/j.bbrc.2018.05.198.

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30

Xiong, Yunhe, Jiabin Zhang, and Chao Song. "CircRNA ZNF609 functions as a competitive endogenous RNA to regulate FOXP4 expression by sponging miR‐138‐5p in renal carcinoma." Journal of Cellular Physiology 234, no. 7 (November 27, 2018): 10646–54. http://dx.doi.org/10.1002/jcp.27744.

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31

Tao, Hong‑Fang, Jia‑Xin Shen, Zhan‑Wen Hou, Shao‑Yan Chen, Yong‑Zhong Su, and Jian‑Lin Fang. "lncRNA FOXP4‑AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR‑423‑5p/NACC1 pathway." Oncology Reports 45, no. 2 (December 11, 2020): 469–80. http://dx.doi.org/10.3892/or.2020.7897.

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32

Long, Qing-Zhi, Yue-Feng Du, Xiao-Ying Ding, Xiang Li, Wen-Bin Song, Yong Yang, Peng Zhang, Jian-Ping Zhou, and Xiao-Gang Liu. "Replication and Fine Mapping for Association of the C2orf43, FOXP4, GPRC6A and RFX6 Genes with Prostate Cancer in the Chinese Population." PLoS ONE 7, no. 5 (May 25, 2012): e37866. http://dx.doi.org/10.1371/journal.pone.0037866.

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33

Li, Hongqing, Qing Zhao, and Zhonghao Tang. "LncRNA RP11-116G8.5 promotes the progression of lung squamous cell carcinoma through sponging miR-3150b-3p/miR-6870-5p to upregulate PHF12/FOXP4." Pathology - Research and Practice 226 (October 2021): 153566. http://dx.doi.org/10.1016/j.prp.2021.153566.

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34

Shu, W., M. M. Lu, Y. Zhang, P. W. Tucker, D. Zhou, and E. E. Morrisey. "Foxp2 and Foxp1 cooperatively regulate lung and esophagus development." Development 134, no. 10 (April 11, 2007): 1991–2000. http://dx.doi.org/10.1242/dev.02846.

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35

Stumm, Laura, Lia Burkhardt, Stefan Steurer, Ronald Simon, Meike Adam, Andreas Becker, Guido Sauter, et al. "Strong expression of the neuronal transcription factor FOXP2 is linked to an increased risk of early PSA recurrence in ERG fusion-negative cancers." Journal of Clinical Pathology 66, no. 7 (April 4, 2013): 563–68. http://dx.doi.org/10.1136/jclinpath-2012-201335.

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Background and aimsTranscription factors of the forkhead box P (FOXP1-4) family have been implicated in various human cancer types before. The relevance and role of neuronal transcription factor FOXP2 in prostate cancer is unknown.MethodsA tissue microarray containing samples from more than 11 000 prostate cancers from radical prostatectomy specimens with clinical follow-up data was analysed for FOXP2 expression by immunohistochemistry. FOXP2 data were also compared with pre-existing ERG fusion (by fluorescence in situ hybridisation and immunohistochemistry) and cell proliferation (Ki67 labelling index) data.ResultsThere was a moderate to strong FOXP2 protein expression in basal and secretory cells of normal prostatic glands. As compared with normal cells, FOXP2 expression was lost or reduced in 25% of cancers. Strong FOXP2 expression was linked to advanced tumour stage, high Gleason score, presence of lymph node metastases and early tumour recurrence (p<0.0001; each) in ERG fusion-negative, but not in ERG fusion-positive cancers. High FOXP2 expression was linked to high Ki67 labelling index (p<0.0001) in all cancers irrespective of ERG fusion status.ConclusionsThese data demonstrate that similar high FOXP2 protein levels as in normal prostate epithelium exert a ‘paradoxical’ oncogenic role in ‘non fusion-type’ prostate cancer. It may be speculated that interaction of FOXP2 with members of pathways that are specifically activated in ‘non fusion-type’ cancers may be responsible for this phenomenon.

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Wu, Jiali, Peng Liu, Hailin Tang, Zeyu Shuang, Qingsheng Qiu, Lijuan Zhang, Cailu Song, Lingrui Liu, Xiaoming Xie, and Xiangsheng Xiao. "FOXP2 Promotes Tumor Proliferation and Metastasis by Targeting GRP78 in Triple-negative Breast Cancer." Current Cancer Drug Targets 18, no. 4 (April 6, 2018): 382–89. http://dx.doi.org/10.2174/1568009618666180131115356.

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Background: FOXP2, a member of the forkhead box P (FOXP) family, has been reported to be important in breast cancer. However, its exact mechanisms and pathways remain unclear. Objective: To investigate the effect of FOXP2 on tumor proliferation and metastasis in triplenegative breast cancer (TNBC) and study its underlying molecular mechanism. Methods: We first used qRT-PCR to detect FOXP2 expression in TNBC cell lines and tissues. Then we conducted cell proliferation assays, colony formation assays, and transwell assays to analyze the effects of FOXP2 expression in TNBC cells. Mouse xenograft model was performed to further confirm the role of FOXP2 in TNBC. Moreover, we used qRT-PCR and Western blot to access the effect of FOXP2 on GRP78 expression and qRT-PCR to analyze GRP78 expression in TNBC tissues. We conducted IHC analysis to detect both FOXP2 and GRP78 expressions in transplanted tumors and used the correlation analysis to further analyze the link between them. Results: FOXP2 was found to be highly expressed in TNBC cell lines and tissues. FOXP2 knockdown attenuated the growth and invasiveness of TNBC in vitro as well as tumor progression and metastasis in vivo. Moreover, FOXP2 knockdown downregulated glucose-regulated protein of molecular mass 78 (GRP78) expression in TNBC cells and transplanted tumors. Correlation analysis showed that GRP78 expression was positively associated with FOXP2 expression in TNBC cells. Conclusion: FOXP2 plays a crucial role in TNBC, partly through modulating GRP78, and could act as a potential target for TNBC treatment.

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37

Morris, Gavin, Stoyan Stoychev, Previn Naicker, Heini W. Dirr, and Sylvia Fanucchi. "The forkhead domain hinge-loop plays a pivotal role in DNA binding and transcriptional activity of FOXP2." Biological Chemistry 399, no. 8 (July 26, 2018): 881–93. http://dx.doi.org/10.1515/hsz-2018-0185.

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Abstract Forkhead box (FOX) proteins are a ubiquitously expressed family of transcription factors that regulate the development and differentiation of a wide range of tissues in animals. The FOXP subfamily members are the only known FOX proteins capable of forming domain-swapped forkhead domain (FHD) dimers. This is proposed to be due to an evolutionary mutation (P539A) that lies in the FHD hinge loop, a key region thought to fine-tune DNA sequence specificity in the FOX transcription factors. Considering the importance of the hinge loop in both the dimerisation mechanism of the FOXP FHD and its role in tuning DNA binding, a detailed investigation into the implications of mutations within this region could provide important insight into the evolution of the FOX family. Isothermal titration calorimetry and hydrogen exchange mass spectroscopy were used to study the thermodynamic binding signature and changes in backbone dynamics of FOXP2 FHD DNA binding. Dual luciferase reporter assays were performed to study the effect that the hinge-loop mutation has on FOXP2 transcriptional activity in vivo. We demonstrate that the change in dynamics of the hinge-loop region of FOXP2 alters the energetics and mechanism of DNA binding highlighting the critical role of hinge loop mutations in regulating DNA binding characteristics of the FOX proteins.

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38

Teramitsu, I. "Parallel FoxP1 and FoxP2 Expression in Songbird and Human Brain Predicts Functional Interaction." Journal of Neuroscience 24, no. 13 (March 31, 2004): 3152–63. http://dx.doi.org/10.1523/jneurosci.5589-03.2004.

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39

Konopacki, Catherine, Yuri Pritykin, Yury Rubtsov, Christina S. Leslie, and Alexander Y. Rudensky. "Transcription factor Foxp1 regulates Foxp3 chromatin binding and coordinates regulatory T cell function." Nature Immunology 20, no. 2 (January 14, 2019): 232–42. http://dx.doi.org/10.1038/s41590-018-0291-z.

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40

Bacon, Claire, and Gudrun A. Rappold. "The distinct and overlapping phenotypic spectra of FOXP1 and FOXP2 in cognitive disorders." Human Genetics 131, no. 11 (June 27, 2012): 1687–98. http://dx.doi.org/10.1007/s00439-012-1193-z.

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41

Cesario, Jeffry M., Asma A. Almaidhan, and Juhee Jeong. "Expression of forkhead box transcription factor genes Foxp1 and Foxp2 during jaw development." Gene Expression Patterns 20, no. 2 (March 2016): 111–19. http://dx.doi.org/10.1016/j.gep.2016.03.001.

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Donizy, Piotr, Cheng-Lin Wu, Janusz Kopczynski, Malgorzata Pieniazek, Przemyslaw Biecek, Janusz Ryś, and Mai P. Hoang. "Prognostic Role of Tumoral PD-L1 and IDO1 Expression, and Intratumoral CD8+ and FoxP3+ Lymphocyte Infiltrates in 132 Primary Cutaneous Merkel Cell Carcinomas." International Journal of Molecular Sciences 22, no. 11 (May 23, 2021): 5489. http://dx.doi.org/10.3390/ijms22115489.

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The association of immune markers and clinicopathologic features and patient outcome has not been extensively studied in Merkel cell carcinoma (MCC). We correlated tumoral PD-L1 and IDO1 expression, and intratumoral CD8+ and FoxP3+ lymphocytes count with clinicopathologic variables, Merkel cell polyomavirus (MCPyV) status, and patient outcomes in a series of 132 MCC. By univariate analyses, tumoral PD-L1 expression >1% and combined tumoral PD-L1 >1% and high intratumoral FoxP3+ lymphocyte count correlated with improved overall survival (OS) (p = 0.016, 0.0072), MCC-specific survival (MSS) (p = 0.019, 0.017), and progression-free survival (PFS) (p = 0.043, 0.004, respectively). High intratumoral CD8+ and FoxP3+ lymphocyte count correlated with longer MSS (p = 0.036) and improved PFS (p = 0.047), respectively. Ulceration correlated with worse OS and worse MSS. Age, male gender, and higher stage (3 and 4) significantly correlated with worse survival. MCPyV positivity correlated with immune response. By multivariate analyses, only ulceration and age remained as independent predictors of worse OS; gender and stage remained for shorter PFS. Tumoral PD-L1 expression and increased density of intratumoral CD8+ lymphocytes and FoxP+ lymphocytes may represent favorable prognosticators in a subset of MCCs. Tumoral PD-L1 expression correlated with intratumoral CD8+ and FoxP3+ lymphocytes, which is supportive of an adaptive immune response.

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Ferland, Russell J., Timothy J. Cherry, Patricia O. Preware, Edward E. Morrisey, and Christopher A. Walsh. "Characterization of Foxp2 and Foxp1 mRNA and protein in the developing and mature brain." Journal of Comparative Neurology 460, no. 2 (May 26, 2003): 266–79. http://dx.doi.org/10.1002/cne.10654.

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Sollis, Elliot, Pelagia Deriziotis, Hirotomo Saitsu, Noriko Miyake, Naomichi Matsumoto, Mariëtte J. V. Hoffer, Claudia A. L. Ruivenkamp, et al. "Equivalent missense variant in the FOXP2 and FOXP1 transcription factors causes distinct neurodevelopmental disorders." Human Mutation 38, no. 11 (August 14, 2017): 1542–54. http://dx.doi.org/10.1002/humu.23303.

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Kumar, Subodh, Ankita Batra, Shruthi Kanthaje, Sujata Ghosh, and Anuradha Chakraborti. "Crosstalk between microRNA-122 and FOX family genes in HepG2 cells." Experimental Biology and Medicine 242, no. 4 (November 28, 2016): 436–40. http://dx.doi.org/10.1177/1535370216681548.

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MicroRNA-122 (miR-122) is liver specific and plays an important role in physiology as well as diseases including hepatocellular carcinoma (HCC). Downregulation of miR-122 in HCC modulates apoptosis. Similarly, the putative targets of miR-122, the forkhead box (FOX) family genes also play an important role in the regulation of apoptosis. Hence, an interplay between miR-122 and FOX family genes has been explored in this study. Initially, an augmentation of apoptosis was noticed in HepG2 cells after transfection with miR-122. Further, the predicted miR-122 targets, the FOX family genes ( FOXM1b, FOXP1, and FOXO4) were selected via in silico analysis based on their role in apoptosis. We checked the expression of all these genes at transcript level after the transfection of miR-122 and found that the relative expression of FOXP1 and FOXM1b was significantly downregulated (p < 0.005) and that of FOXO4 was upregulated (p < 0.005). Thus, the finding indicates deregulation of these FOX genes as a result of miR-122 augmentation might be involved in the modulation of apoptosis. Impact Statement Here, we have investigated the crosstalk between microRNA-122 (miR-122) and selective FOX family genes in HepG2 cells. miR-122 is a prominent miRNA in liver and has been reported to be downregulated in hepatocellular carcinoma (HCC). It has been speculated that diminished level of miR-122 during HCC might be one of the reasons for tumor progression. However, the exact molecular interactions are not clear yet. This study unravels one of the molecular mechanisms of miR-122 through which it might impact the tumorigenesis of HCC.

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Hisaoka, Tomoko, Yoshihiro Morikawa, and Emiko Senba. "Different expression pattern of Foxp1 and Foxp2 in the mouse cerebral cortex during postnatal development." Neuroscience Research 68 (January 2010): e362. http://dx.doi.org/10.1016/j.neures.2010.07.1605.

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Hara, Erina, Jemima M. Perez, Osceola Whitney, Qianqian Chen, Stephanie A. White, and Timothy F. Wright. "Neural FoxP2 and FoxP1 expression in the budgerigar, an avian species with adult vocal learning." Behavioural Brain Research 283 (April 2015): 22–29. http://dx.doi.org/10.1016/j.bbr.2015.01.017.

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Fong, Weng Lam, Hsiao-Ying Kuo, Hsiao-Lin Wu, Shih-Yun Chen, and Fu-Chin Liu. "Differential and Overlapping Pattern of Foxp1 and Foxp2 Expression in the Striatum of Adult Mouse Brain." Neuroscience 388 (September 2018): 214–23. http://dx.doi.org/10.1016/j.neuroscience.2018.07.017.

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Rappold, G. A., Henning Fröhlich, Rafiullah Rafiullah, Nathalie Schmitt, and Sonja Abele. "Sex-Specific Foxp1 And Foxp2 Expression In The Developing Mouse Brain And Its Impact on Vocal Communication." European Neuropsychopharmacology 27 (2017): S372. http://dx.doi.org/10.1016/j.euroneuro.2016.09.400.

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Bakshi, Nasir, Rami Albugami, Abdulmonem Almutawa, Mohammed Alghamdi, Irfan Maghfoor, and Saad Akhter. "FOXP3 Can Predict Disease Progression and Risk of Transformation in Uniformly Treated Patients with Mycosis Fungoides." Blood 118, no. 21 (November 18, 2011): 5182. http://dx.doi.org/10.1182/blood.v118.21.5182.5182.

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Abstract Abstract 5182 Background: Mycosis fungoides (MF) is a heterogeneous lymphoid neoplasm with a variable clinical course. In early stages MF often runs an indolent course. A small but significant part of these patients develop an aggressive course frequently associated with inferior survival. No consistent biological markers are predictive of survival or risk of transformation (RT). Foxp3 belongs to a novel forkhead transcription factor essential for the development and regulation of regulatory T-cells (Treg). Recent studies have shown conflicting results when expression of Foxp3 was analyzed as a prognostic factor in MF. We hypothesized that Foxp3 could be an important marker in predicting for overall survival (OS), progression-free (PFS) survival and RT in MF patients managed by uniform treatment regimens. Methods: 42 patients with newly diagnosed MF were retrieved form the record files. All patients were managed and treated at our institute. Complete follow-up and pathological material (paraffin blocks) was available for 35/42 patients. In all 35 cases the diagnostic biopsies were reviewed concurrently by an expert dermatopathologist and hematopathologist and diagnosis fully confirmed. The diagnostic biopsies were immunostained with CD3, CD4, CD7, CD8, CD30 and CD56 specific antibodies. Clonality for TCR gamma was performed for most of the cases in the study (85%). FOXP3 antibody (clone 221D/D3) that recognizes the Foxp3 in the nucleus (but does not cross react with other Foxp proteins) was utilized for studying the Foxp3 expression by the tumor cells and or peritumoral lymphocytes. 20 cases of reactive non-neoplastic dermal lesions including lichen planus, lupus and dermatitis were also immunostained for Foxp3 for comparison. Only high intensity nuclear staining was accepted as positive expression. The Foxp3 staining was further semi quantitatively estimated as no expression (0), 0–10% (1+), 10–50% (2+) and >50% (3+). Both the cell content and immuno-architectureal pattern were determined. Age, sex, clinical presentation, stage of disease was compared to Fox3 expression by chi-square and Fishers's exact test. The Kaplan-Meyer method and log rank test were used to evaluate survival data. Results: 34 of 35 (97%) patients were alive at 8 years. Tumor stage at the time of diagnosis as defined by ISCL-EORTC, 2008 was as follows: stage 1A (57%), 1B (25%), 2A (6%), 2B (6%), 3 (6%). 19/35 (54%) were female and 16/35 (46%) were male. The median age at diagnosis was 44.0 years (range 7–80 years). The median follow-up period was 37 months (range 12– 96 months). Foxp3 expression showed predominantly intraepidermal or basal localization of tumor cells. In most of the cases the epidermotropism and the nuclear atypia was helpful in easily discerning tumor cells from reactive non-neoplastic Tregs. Reactive dermal lesions served as an excellent control in that the distribution of Tregs in these lesions was predominantly dermal and rarely basal. Overall 28/35 (80%) and 7/35 (20%) cases were positive and negative for Foxp3 respectively. There was no significant correlation between disease pattern, clinical presentation, stage, age or sex and marker expression. In the Foxp3 positive patients 17/28(61%) showed disease progression whereas 11/28 (39%) were free of disease at last follow-up (FU period 12–96 months) (p=0.05, Fisher's exact test). 13/28 (46%) Foxp3+ patients were found to have relapse of disease after initial response compared to only 2/7 (28.5%) patients, who relapsed but lacked Foxp3 expression (p=0.242, Fisher's exact test). Comparing disease progression and aggressiveness as evidenced by lymph node metastasis and transformation to Sezary syndrome: only Foxp3 positive cases (4 versus 0) had evidence of disease progression (3 lymph node metastasis alone and one Sezary syndrome) thus indicating increased RT. One patient who died of widespread disease showed >30% Foxp3 expression in the neoplastic lymphoid cells. Conclusions: Specific biological markers for outcome and prognosis in MF remain elusive. A regulatory T-cell (Treg) phenotype defines a subset of MF patients who might carry a different prognosis and might require more aggressive and or targeted therapy. More data on Foxp3 expression in cutaneous T-cell lymphomas and its clinical significance is needed. Disclosures: No relevant conflicts of interest to declare.

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