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Journal articles on the topic 'Cancer Enzymes'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Schwartz, Morton K. "Enzymes in Cancer." Clinics in Laboratory Medicine 9, no. 4 (1989): 757–66. http://dx.doi.org/10.1016/s0272-2712(18)30603-6.

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2

Tran, Luyen Van. "ID2018 Radioisotope Enzymes And Cancer Study." Biomedical Research and Therapy 4, S (2017): 51. http://dx.doi.org/10.15419/bmrat.v4is.261.

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Cancer is a pathological symptom, when abnormal cells appear in certain human tissues or organs. These cells can reproduce beyond the control of normal biological protection mechanism. Because they multiply themselves rapidly, the metabolic process is accelerated, which causes an extreme need for energy, substrate material and catalyzing enzyme. Bases on these needs, we can control the metabolic process by: • Stopping the supply of energy. • Stopping the supply of substrate materials to build up the cell’s structure. • Stopping the catalysis process by breaking out the enzyme’s structure and/o

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3

Mohamed, Mona Mostafa, and Bonnie F. Sloane. "multifunctional enzymes in cancer." Nature Reviews Cancer 6, no. 10 (2006): 764–75. http://dx.doi.org/10.1038/nrc1949.

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4

Asaduzzaman Khan, Md, Mousumi Tania, Dian-zheng Zhang, and Han-chun Chen. "Antioxidant enzymes and cancer." Chinese Journal of Cancer Research 22, no. 2 (2010): 87–92. http://dx.doi.org/10.1007/s11670-010-0087-7.

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5

Pramono, Alvinsyah Adhityo, Gulam M. Rather, Herry Herman, Keri Lestari, and Joseph R. Bertino. "NAD- and NADPH-Contributing Enzymes as Therapeutic Targets in Cancer: An Overview." Biomolecules 10, no. 3 (2020): 358. http://dx.doi.org/10.3390/biom10030358.

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Actively proliferating cancer cells require sufficient amount of NADH and NADPH for biogenesis and to protect cells from the detrimental effect of reactive oxygen species. As both normal and cancer cells share the same NAD biosynthetic and metabolic pathways, selectively lowering levels of NAD(H) and NADPH would be a promising strategy for cancer treatment. Targeting nicotinamide phosphoribosyltransferase (NAMPT), a rate limiting enzyme of the NAD salvage pathway, affects the NAD and NADPH pool. Similarly, lowering NADPH by mutant isocitrate dehydrogenase 1/2 (IDH1/2) which produces D-2-hydrox

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6

Marquez, Jubert, Jessa Flores, Amy Hyein Kim, et al. "Rescue of TCA Cycle Dysfunction for Cancer Therapy." Journal of Clinical Medicine 8, no. 12 (2019): 2161. http://dx.doi.org/10.3390/jcm8122161.

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Mitochondrion, a maternally hereditary, subcellular organelle, is the site of the tricarboxylic acid (TCA) cycle, electron transport chain (ETC), and oxidative phosphorylation (OXPHOS)—the basic processes of ATP production. Mitochondrial function plays a pivotal role in the development and pathology of different cancers. Disruption in its activity, like mutations in its TCA cycle enzymes, leads to physiological imbalances and metabolic shifts of the cell, which contributes to the progression of cancer. In this review, we explored the different significant mutations in the mitochondrial enzymes

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7

Jabbour, H. N. "007. INFLAMMATORY PATHWAYS IN ENDOMETRIAL CANCER." Reproduction, Fertility and Development 21, no. 9 (2009): 5. http://dx.doi.org/10.1071/srb09abs007.

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Endometrial cancer is the most common gynaecological malignancy and accounts for 5% of cancers in women (http://info.cancerresearchuk.org/cancerstats/). The majority of endometrial cancers occur in post-menopausal women and 80% of patients are diagnosed when the tumour is confined to the uterus (stage 1 disease). Many of the risk factors for developing endometrial cancer are associated with excess exposure to oestrogen unopposed by progesterone. It is well established that local inflammatory pathways contribute to the initiation and progression of endometrial cancers via the release of local m

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8

Bui, Quyen Thu, Jeong Hee Hong, Minseok Kwak, Ji Yeon Lee, and Peter Chang-Whan Lee. "Ubiquitin-Conjugating Enzymes in Cancer." Cells 10, no. 6 (2021): 1383. http://dx.doi.org/10.3390/cells10061383.

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The ubiquitin-mediated degradation system is responsible for controlling various tumor-promoting processes, including DNA repair, cell cycle arrest, cell proliferation, apoptosis, angiogenesis, migration and invasion, metastasis, and drug resistance. The conjugation of ubiquitin to a target protein is mediated sequentially by the E1 (activating)‒E2 (conjugating)‒E3 (ligating) enzyme cascade. Thus, E2 enzymes act as the central players in the ubiquitination system, modulating various pathophysiological processes in the tumor microenvironment. In this review, we summarize the types and functions

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9

Al-Ghurabi, Batool Hassan, Abeer Khalid Yaseen, and Mohammed Imran Hamzah. "Serum Levels of Lactate Dehydrogenase and Alkaline Phosphatase Enzymes in Colorectal Cancer." Journal of Pure and Applied Microbiology 13, no. 1 (2019): 475–79. http://dx.doi.org/10.22207/jpam.13.1.53.

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10

Ramarao-Milne, Priya, Olga Kondrashova, Sinead Barry, John D. Hooper, Jason S. Lee, and Nicola Waddell. "Histone Modifying Enzymes in Gynaecological Cancers." Cancers 13, no. 4 (2021): 816. http://dx.doi.org/10.3390/cancers13040816.

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Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant of chromosomal conformation and stability, and unlike DNA methylation, which is generally associated with gene silencing, are amenable to post-translational modifications that induce facultative chromatin regions, or condensed transcriptionally silent regions that decondense res

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11

Feng, Siqi, Anqi Li, Yi-Chao Zheng, and Hong-Min Liu. "Role of Drug-metabolizing Enzymes in Cancer and Cancer Therapy." Current Drug Metabolism 21, no. 1 (2020): 67–76. http://dx.doi.org/10.2174/1389200221666200103111053.

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Background: Cancer is one of the most serious diseases threatening human health with high morbidity and mortality in the world. For the treatment of cancer, chemotherapy is one of the most widely used strategies, for almost all kinds of tumors and diverse stages of tumor development. The efficacy of chemotherapy not only depends on the activity of the drug administrated but also on whether the compound could reach the effective therapeutic concentration in tumor cells. Therefore, expression and activity of drug-metabolizing enzymes (DMEs) in tumor tissues and metabolic organs of cancer patient

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12

Wright, Roni H. G., and Miguel Beato. "Role of the NUDT Enzymes in Breast Cancer." International Journal of Molecular Sciences 22, no. 5 (2021): 2267. http://dx.doi.org/10.3390/ijms22052267.

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Despite global research efforts, breast cancer remains the leading cause of cancer death in women worldwide. The majority of these deaths are due to metastasis occurring years after the initial treatment of the primary tumor and occurs at a higher frequency in hormone receptor-positive (Estrogen and Progesterone; HR+) breast cancers. We have previously described the role of NUDT5 (Nudix-linked to moiety X-5) in HR+ breast cancer progression, specifically with regards to the growth of breast cancer stem cells (BCSCs). BCSCs are known to be the initiators of epithelial-to-mesenchyme transition (

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13

Granadillo Rodríguez, Milaid, Ben Flath, and Linda Chelico. "The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead." Open Biology 10, no. 12 (2020): 200188. http://dx.doi.org/10.1098/rsob.200188.

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Cancer is considered a group of diseases characterized by uncontrolled growth and spread of abnormal cells and is propelled by somatic mutations. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) family of enzymes are endogenous sources of somatic mutations found in multiple human cancers. While these enzymes normally act as an intrinsic immune defence against viruses, they can also catalyse ‘off-target’ cytidine deamination in genomic single-stranded DNA intermediates. The deamination of cytosine forms uracil, which is promutagenic in DNA. Key factors to trigger the

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14

Tao, Zijia, Yiqiao Zhao, and Xiaonan Chen. "Role of methyltransferase-like enzyme 3 and methyltransferase-like enzyme 14 in urological cancers." PeerJ 8 (July 22, 2020): e9589. http://dx.doi.org/10.7717/peerj.9589.

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N6-methyladenosine (m6A) modifications can be found in eukaryotic messenger RNA (mRNA), long non-coding RNA (lncRNA), and microRNA (miRNA). Several studies have demonstrated a close relationship between m6A modifications and cancer cells. Methyltransferase-like enzyme 3 (METTL3) and methyltransferase-like enzyme 14 (METTL14) are two major enzymes involved in m6A modifications that play vital roles in various cancers. However, the roles and regulatory mechanisms of METTL3 and METTL14 in urological cancers are largely unknown. In this review, we summarize the current research results for METTL3

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15

Deonarain, MP, and AA Epenetos. "Targeting enzymes for cancer therapy: old enzymes in new roles." British Journal of Cancer 70, no. 5 (1994): 786–94. http://dx.doi.org/10.1038/bjc.1994.400.

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16

Nakamura, Yasuhiro, Takashi Suzuki, Masao Nakabayashi, et al. "In situ androgen producing enzymes in human prostate cancer." Endocrine-Related Cancer 12, no. 1 (2005): 101–7. http://dx.doi.org/10.1677/erc.1.00914.

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Androgens have been proposed to be actively produced in situ in human prostate cancer. These locally produced androgens have also been considered to play important roles in the pathogenesis and development of prostate cancer. Therefore, it is important to examine the status of this in situ androgen metabolism and/or synthesis in detail in order to improve the clinical response to hormonal therapy in patients diagnosed with prostate cancer. Several studies have previously demonstrated the expression of androgen-producing enzymes such as 5α-reductase types 1 and 2, and 17β-hydroxysteroid dehydro

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17

Raza, Uzma, Aziza Khannum, and Shahnawaz Jamali. "LIVER ENZYMES." Professional Medical Journal 22, no. 06 (2015): 745–51. http://dx.doi.org/10.29309/tpmj/2015.22.06.1242.

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Objective: To study the effect of breast cancer treatment on liver enzymes indiabetic and cardiac breast cancer females. Study Design: Cross-sectional type of study.Setting: Liaquat National Hospital Karachi. Period: January 2008 to January 2010. Patientsand Methods: Total 47 breast cancer patients. Out of these, 22 were diabetic and 25 werecardiac patients, visiting the oncology OPD of the hospital. Patients with metastasis to distantorgans were excluded from the study. Treatment was carried under the supervision of anoncologist. Samples were collected twice during the study. First sample was

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18

Akbari, Masoud, Emrullah Sogutdelen, Smriti Juriasingani, and Alp Sener. "Hydrogen Sulfide: Emerging Role in Bladder, Kidney, and Prostate Malignancies." Oxidative Medicine and Cellular Longevity 2019 (November 3, 2019): 1–10. http://dx.doi.org/10.1155/2019/2360945.

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Hydrogen sulfide (H2S) is the latest member of the gasotransmitter family and known to play essential roles in cancer pathophysiology. H2S is produced endogenously and can be administered exogenously. Recent studies showed that H2S in cancers has both pro- and antitumor roles. Understanding the difference in the expression and localization of tissue-specific H2S-producing enzymes in healthy and cancer tissues allows us to develop tools for cancer diagnosis and treatment. Urological malignancies are some of the most common cancers in both men and women, and their early detection is vital since

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19

Wang, Haiwei, Xinrui Wang, Liangpu Xu, Ji Zhang, and Hua Cao. "High expression levels of pyrimidine metabolic rate–limiting enzymes are adverse prognostic factors in lung adenocarcinoma: a study based on The Cancer Genome Atlas and Gene Expression Omnibus datasets." Purinergic Signalling 16, no. 3 (2020): 347–66. http://dx.doi.org/10.1007/s11302-020-09711-4.

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Abstract Reprogramming of metabolism is described in many types of cancer and is associated with the clinical outcomes. However, the prognostic significance of pyrimidine metabolism signaling pathway in lung adenocarcinoma (LUAD) is unclear. Using the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets, we found that the pyrimidine metabolism signaling pathway was significantly enriched in LUAD. Compared with normal lung tissues, the pyrimidine metabolic rate–limiting enzymes were highly expressed in lung tumor tissues. The high expression levels of pyrimidine metabolic–r

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20

Fahey, Jed W., and Paul Talalay. "Cancer Chemoprotective Effects of Cruciferous Vegetables." HortScience 31, no. 4 (1996): 696d—696. http://dx.doi.org/10.21273/hortsci.31.4.696d.

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High fruit and vegetable consumption is associated with a striking reduction in susceptibility to malignancy. In addition to other health benefits (e.g., high levels of vitamin C, carotenoids, and dietary fiber), cruciferous vegetables contribute significantly to this chemoprotective effect. Cruciferous vegetables (e.g. Brassica sp.), contain glucosinolates, water-soluble secondary metabolites that are converted to highly reactive isothiocyanates as a defense response to predation or injury. When fed to mammals, isothiocyanates induce Phase 2 enzymes such as glutathione-S-transferase and quino

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21

Malarz, Katarzyna, Jacek Mularski, Marcin Pacholczyk, and Robert Musiol. "The Landscape of the Anti-Kinase Activity of the IDH1 Inhibitors." Cancers 12, no. 3 (2020): 536. http://dx.doi.org/10.3390/cancers12030536.

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Isocitrate dehydrogenases constitute a class of enzymes that are crucial for cellular metabolism. The overexpression or mutation of isocitrate dehydrogenases are often found in leukemias, glioblastomas, lung cancers, and ductal pancreatic cancer among others. Mutation R132H, which changes the functionality of an enzyme to produce mutagenic 2-hydroxyglutarate instead of a normal product, is particularly important in this field. A series of inhibitors were described for these enzymes of which ivosidenib was the first to be approved for treating leukemia and bile duct cancers in 2018. Here, we in

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22

Bednarz-Misa, Iwona, Mariusz G. Fleszar, Paulina Fortuna, et al. "Altered L-Arginine Metabolic Pathways in Gastric Cancer: Potential Therapeutic Targets and Biomarkers." Biomolecules 11, no. 8 (2021): 1086. http://dx.doi.org/10.3390/biom11081086.

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There is a pressing need for molecular targets and biomarkers in gastric cancer (GC). We aimed at identifying aberrations in L-arginine metabolism with therapeutic and diagnostic potential. Systemic metabolites were quantified using mass spectrometry in 293 individuals and enzymes’ gene expression was quantified in 29 paired tumor-normal samples using qPCR and referred to cancer pathology and molecular landscape. Patients with cancer or benign disorders had reduced systemic arginine, citrulline, and ornithine and elevated symmetric dimethylarginine and dimethylamine. Citrulline and ornithine d

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23

Shackelford, Rodney E., Islam Z. Mohammad, Andrew T. Meram, et al. "Molecular Functions of Hydrogen Sulfide in Cancer." Pathophysiology 28, no. 3 (2021): 437–56. http://dx.doi.org/10.3390/pathophysiology28030028.

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Hydrogen sulfide (H2S) is a gasotransmitter that exerts a multitude of functions in both physiologic and pathophysiologic processes. H2S-synthesizing enzymes are increased in a variety of human malignancies, including colon, prostate, breast, renal, urothelial, ovarian, oral squamous cell, and thyroid cancers. In cancer, H2S promotes tumor growth, cellular and mitochondrial bioenergetics, migration, invasion, angiogenesis, tumor blood flow, metastasis, epithelia–mesenchymal transition, DNA repair, protein sulfhydration, and chemotherapy resistance Additionally, in some malignancies, increased

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24

Adnan Yasseen, Hadeel, Rawand Tajuldeen Sahib, and Shaho Abdulrehman Ezzaddin. "MITOCHONDRIAL ENZYMES CORRELATION WITH BREAST CANCER CLINICOPATHOLOGICAL PARAMETERS/ A STUDY IN SULAIMANI CITY-IRAQ." Journal of Sulaimani Medical College 8, no. 1 (2018): 37–46. http://dx.doi.org/10.17656/jsmc.10149.

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25

Komori, Shuji, Shinji Osada, and Kazuhiro Yoshida. "Novel Strategy with Gemcitabine for Advanced Pancreatic Cancer." ISRN Oncology 2011 (May 23, 2011): 1–5. http://dx.doi.org/10.5402/2011/936893.

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5-fluorouracil (5-FU) is widely used in chemotherapy for gastric and colorectal cancer, but gemcitabine (GEM), and not 5-FU, is approved as a standard drug for use in pancreatic cancer. Interindividual variation in the enzyme activity of the GEM metabolic pathway can affect the extent of GEM metabolism and the efficacy of GEM chemotherapy. Human equilibrative nucleoside transporter 1 (hENT1) is recognized as a major transporter of GEM into cells. In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates

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26

BRENNAN, MAIRIN. "Enzymes implicated in arthritis, cancer clarified." Chemical & Engineering News 77, no. 23 (1999): 10. http://dx.doi.org/10.1021/cen-v077n023.p010.

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27

Wojcieszyńska, Danuta, Katarzyna Hupert-Kocurek, and Urszula Guzik. "Flavin-Dependent Enzymes in Cancer Prevention." International Journal of Molecular Sciences 13, no. 12 (2012): 16751–68. http://dx.doi.org/10.3390/ijms131216751.

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28

Kiberstis, P. A. "Enzymes Adopt New M.O. in Cancer." Science 327, no. 5971 (2010): 1305. http://dx.doi.org/10.1126/science.327.5971.1305-b.

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29

Yunis, J. J., and W. R. Hoffman. "Nuclear Enzymes, Fragile Sites, and Cancer." Journal of Gerontology 44, no. 6 (1989): 37–44. http://dx.doi.org/10.1093/geronj/44.6.37.

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30

Encell, Lance P., Daniel M. Landis, and Lawrence A. Loeb. "Improving enzymes for cancer gene therapy." Nature Biotechnology 17, no. 2 (1999): 143–47. http://dx.doi.org/10.1038/6142.

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31

Visnes, Torkild, Maurice Grube, Bishoy Magdy Fekry Hanna, Carlos Benitez-Buelga, Armando Cázares-Körner, and Thomas Helleday. "Targeting BER enzymes in cancer therapy." DNA Repair 71 (November 2018): 118–26. http://dx.doi.org/10.1016/j.dnarep.2018.08.015.

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32

Schwartz, Morton K. "Enzymes in colon cancer. General information." Cancer 36, S6 (2006): 2334–36. http://dx.doi.org/10.1002/1097-0142(197512)36:6<2334::aid-cncr2820360609>3.0.co;2-g.

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33

Suzuki, Takashi, Yasuhiro Miki, Yasuhiro Nakamura, et al. "Sex steroid-producing enzymes in human breast cancer." Endocrine-Related Cancer 12, no. 4 (2005): 701–20. http://dx.doi.org/10.1677/erc.1.00834.

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It is well known that sex steroids are involved in the growth of breast cancers, and the great majority of breast carcinomas express estrogen (ER), progesterone (PR), and androgen (AR) receptors. In particular, recent studies have demonstrated that estrogens and androgens are locally produced in breast carcinoma tissues, and total blockade of in situ estrogen production potentially leads to an improvement in prognosis of breast cancer patients. Therefore, it is important to obtain a better understanding of sex steroid-producing enzymes in breast carcinoma tissues. In this review, we summarize

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34

Liu, Sitong, Lichun Wang, Dongjun Jiang, et al. "Sumoylation as an Emerging Target in Therapeutics against Cancer." Current Pharmaceutical Design 26, no. 37 (2020): 4764–76. http://dx.doi.org/10.2174/1381612826666200622124134.

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Sumoylation is the Post-translational modification gaining most of the research interest recently. Sumoylation is involved in various crucial functions of the cell such as regulation of cell cycle, DNA damage repair, apoptosis, etc. Oncology is advancing in radiotherapy, targeted chemotherapy, various forms of immunotherapy and targeted gene therapy. Researches are being conducted to prove its connotation with a variety of cancers and inhibitors are being developed to obstruct the fatal effect caused by misbalance of the SUMO-catalytic cycle. It has been shown that up-regulation of certain enz

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35

Jones, Wilson, Thomas, Gaughan, and Wade. "The Histone Demethylase Enzymes KDM3A and KDM4B Co-Operatively Regulate Chromatin Transactions of the Estrogen Receptor in Breast Cancer." Cancers 11, no. 8 (2019): 1122. http://dx.doi.org/10.3390/cancers11081122.

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Many estrogen receptor (ER)-positive breast cancers develop resistance to endocrine therapy but retain canonical receptor signalling in the presence of selective ER antagonists. Numerous co-regulatory proteins, including enzymes that modulate the chromatin environment, control the transcriptional activity of the ER. Targeting ER co-regulators has therefore been proposed as a novel therapeutic approach. By assessing DNA-binding dynamics in ER-positive breast cancer cells, we have identified that the histone H3 lysine 9 demethylase enzymes, KDM3A and KDM4B, co-operate to regulate ER activity via

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36

Kincaid, John WR, and Nathan A. Berger. "NAD metabolism in aging and cancer." Experimental Biology and Medicine 245, no. 17 (2020): 1594–614. http://dx.doi.org/10.1177/1535370220929287.

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NAD+ and its derivatives NADH, NADP+, and NADPH are essential cofactors in redox reactions and electron transport pathways. NAD serves also as substrate for an extensive series of regulatory enzymes including cyclic ADP-ribose hydrolases, mono(ADP-ribosyl)transferases, poly(ADP-ribose) polymerases, and sirtuin deacetylases which are O-acetyl-ADP-ribosyltransferases. As a result of the numerous and diverse enzymes that utilize NAD as well as depend on its synthesis and concentration, significant interest has developed in its role in a variety of physiologic and pathologic processes, and therape

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37

Laurenti, Giulio, and Daniel A. Tennant. "Isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH), fumarate hydratase (FH): three players for one phenotype in cancer?" Biochemical Society Transactions 44, no. 4 (2016): 1111–16. http://dx.doi.org/10.1042/bst20160099.

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In the early 1920s Otto Warburg observed that cancer cells have altered metabolism and from this, posited that mitochondrial dysfunction underpinned the aetiology of cancers. The more recent identification of mutations of mitochondrial metabolic enzymes in a wide range of human cancers has now provided a direct link between metabolic alterations and cancer. In this review we discuss the consequences of dysfunction of three metabolic enzymes involved in or associated with the tricarboxylic acid (TCA) cycle: succinate dehydrogenase (SDH), fumarate hydratase (FH) and isocitrate dehydrogenase (IDH

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Nguyen, Yen T. K., Joon Sung Park, Jun Young Jang, et al. "Structural and Functional Analyses of Human ChaC2 in Glutathione Metabolism." Biomolecules 10, no. 1 (2019): 31. http://dx.doi.org/10.3390/biom10010031.

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Glutathione (GSH) degradation plays an essential role in GSH homeostasis, which regulates cell survival, especially in cancer cells. Among human GSH degradation enzymes, the ChaC2 enzyme acts on GSH to form 5-l-oxoproline and Cys-Gly specifically in the cytosol. Here, we report the crystal structures of ChaC2 in two different conformations and compare the structural features with other known γ-glutamylcyclotransferase enzymes. The unique flexible loop of ChaC2 seems to function as a gate to achieve specificity for GSH binding and regulate the constant GSH degradation rate. Structural and bioch

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Chang, Caroline, Beth L. Worley, Rébécca Phaëton, and Nadine Hempel. "Extracellular Glutathione Peroxidase GPx3 and Its Role in Cancer." Cancers 12, no. 8 (2020): 2197. http://dx.doi.org/10.3390/cancers12082197.

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Mammalian cells possess a multifaceted antioxidant enzyme system, which includes superoxide dismutases, catalase, the peroxiredoxin/thioredoxin and the glutathione peroxidase systems. The dichotomous role of reactive oxygen species and antioxidant enzymes in tumorigenesis and cancer progression complicates the use of small molecule antioxidants, pro-oxidants, and targeting of antioxidant enzymes as therapeutic approaches for cancer treatment. It also highlights the need for additional studies to investigate the role and regulation of these antioxidant enzymes in cancer. The focus of this revie

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40

Ardiani, Andressa, Adam J. Johnson, Hongmei Ruan, Marilyn Sanchez-Bonilla, Kinta Serve, and Margaret E. Black. "Enzymes To Die For: Exploiting Nucleotide Metabolizing Enzymes for Cancer Gene Therapy." Current Gene Therapy 12, no. 2 (2012): 77–91. http://dx.doi.org/10.2174/156652312800099571.

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41

Makar, Subhajit, Abhrajyoti Ghosh, Ashok Kumar, and Sushil K. Singh. "Recent Studies on Aromatase and Sulfatase Involved in Breast Cancer and their Inhibitors." Current Enzyme Inhibition 16, no. 1 (2020): 20–44. http://dx.doi.org/10.2174/1573408016666200325120248.

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Enzyme aromatase uses several androgen substrates for the biosynthesis of estrogen, i.e. conversion of androstenedione to estrone and testosterone to biologically potent estradiol. Aromatase inhibitors (AIs) such as anastrozole, letrozole and exemestane have been established in standard endocrine therapy of breast cancer, by interfering with estrogen signaling cascade. Steroid sulphatase (STS) regulates the level of active oestrogens and androgens in human target organs and steroidogenic tissues, which have a key role in hormone dependent breast cancers (HDBC). Sulfatase is still under the exp

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42

Yasinzai, Masoom. "Quantitation of the Cancer Marker LASA Using Immobilized Enzymes in a Semiautomated System." International Journal of Biological Markers 24, no. 2 (2009): 107–11. http://dx.doi.org/10.1177/172460080902400207.

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Cancer patients are found to have elevated serum levels of lipid-associated sialic acid (LASA). LASA measurement provides a valuable test for the diagnosis of human cancer. The currently used measurement methods are tedious and nonselective. Here we report a method based on immobilized enzyme minicolumns in a flow system for the analysis of this clinically important analyte. Three enzymes comprising two minicolumns are introduced online and the analyte in a precisely injected volume of 20 μL is made to pass through these immobilized enzyme columns. The final product of the reaction is detected

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43

Mohammad, Goran Hamid, Vessela Vassileva, Pilar Acedo, et al. "Targeting Pyruvate Kinase M2 and Lactate Dehydrogenase A Is an Effective Combination Strategy for the Treatment of Pancreatic Cancer." Cancers 11, no. 9 (2019): 1372. http://dx.doi.org/10.3390/cancers11091372.

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Reprogrammed glucose metabolism is one of the hallmarks of cancer, and increased expression of key glycolytic enzymes, such as pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA), has been associated with poor prognosis in various malignancies. Targeting these enzymes could attenuate aerobic glycolysis and inhibit tumor proliferation. We investigated whether the PKM2 activator, TEPP-46, and the LDHA inhibitor, FX-11, can be combined to inhibit in vitro and in vivo tumor growth in preclinical models of pancreatic cancer. We assessed PKM2 and LDHA expression, enzyme activity, and cell p

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44

Wang, Dian, Fan Bu, and Weiwei Zhang. "The Role of Ubiquitination in Regulating Embryonic Stem Cell Maintenance and Cancer Development." International Journal of Molecular Sciences 20, no. 11 (2019): 2667. http://dx.doi.org/10.3390/ijms20112667.

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Ubiquitination regulates nearly every aspect of cellular events in eukaryotes. It modifies intracellular proteins with 76-amino acid polypeptide ubiquitin (Ub) and destines them for proteolysis or activity alteration. Ubiquitination is generally achieved by a tri-enzyme machinery involving ubiquitin activating enzymes (E1), ubiquitin conjugating enzymes (E2) and ubiquitin ligases (E3). E1 activates Ub and transfers it to the active cysteine site of E2 via a transesterification reaction. E3 coordinates with E2 to mediate isopeptide bond formation between Ub and substrate protein. The E1-E2-E3 c

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Roy, Roopali, Jiang Yang, and Marsha A. Moses. "Matrix Metalloproteinases As Novel Biomarker s and Potential Therapeutic Targets in Human Cancer." Journal of Clinical Oncology 27, no. 31 (2009): 5287–97. http://dx.doi.org/10.1200/jco.2009.23.5556.

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The matrix metalloproteinase (MMP) family of enzymes is comprised of critically important extracellular matrix remodeling proteases whose activity has been implicated in a number of key normal and pathologic processes. The latter include tumor growth, progression, and metastasis as well as the dysregulated angiogenesis that is associated with these events. As a result, these proteases have come to represent important therapeutic and diagnostic targets for the treatment and detection of human cancers. In this review, we summarize the literature that establishes these enzymes as important clinic

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Filler, Kristin, Debra Lyon, Nancy McCain, et al. "Relationship of Mitochondrial Enzymes to Fatigue Intensity in Men With Prostate Cancer Receiving External Beam Radiation Therapy." Biological Research For Nursing 18, no. 3 (2015): 274–80. http://dx.doi.org/10.1177/1099800415617848.

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Purpose: Mitochondrial dysfunction is a plausible biological mechanism for cancer-related fatigue. Specific aims of this study were to (1) describe the levels of mitochondrial oxidative phosphorylation complex (MOPC) enzymes, fatigue, and health-related quality of life (HRQOL) before and at completion of external beam radiation therapy (EBRT) in men with nonmetastatic prostate cancer (PC); (2) examine relationships over time among levels of MOPC enzymes, fatigue, and HRQOL; and (3) compare levels of MOPC enzymes in men with clinically significant and nonsignificant fatigue intensification duri

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Ershov, Pavel, Leonid Kaluzhskiy, Yuri Mezentsev, Evgeniy Yablokov, Oksana Gnedenko, and Alexis Ivanov. "Enzymes in the Cholesterol Synthesis Pathway: Interactomics in the Cancer Context." Biomedicines 9, no. 8 (2021): 895. http://dx.doi.org/10.3390/biomedicines9080895.

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A global protein interactome ensures the maintenance of regulatory, signaling and structural processes in cells, but at the same time, aberrations in the repertoire of protein–protein interactions usually cause a disease onset. Many metabolic enzymes catalyze multistage transformation of cholesterol precursors in the cholesterol biosynthesis pathway. Cancer-associated deregulation of these enzymes through various molecular mechanisms results in pathological cholesterol accumulation (its precursors) which can be disease risk factors. This work is aimed at systematization and bioinformatic analy

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Hofland, Johannes, Wytske M. van Weerden, Guido Jenster, Fritz H. Schröder, and Frank H. de Jong. "Intraprostatic Steroidogenic Enzymes – Response." Cancer Research 70, no. 20 (2010): 8249–50. http://dx.doi.org/10.1158/0008-5472.can-10-2476.

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Harrington, William R., Surojeet Sengupta, and Benita S. Katzenellenbogen. "Estrogen Regulation of the Glucuronidation Enzyme UGT2B15 in Estrogen Receptor-Positive Breast Cancer Cells." Endocrinology 147, no. 8 (2006): 3843–50. http://dx.doi.org/10.1210/en.2006-0358.

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Estrogens and androgens influence many properties of breast cancer cells; hence, regulation of local estrogen and androgen levels by enzymes involved in steroid hormone biosynthesis and metabolism would impact signaling by these hormones in breast cancer cells. In this study, we show that the UDP-glucuronosyltransferase (UGT) enzyme UGT2B15, a member of the UGT family of phase II enzymes involved in the glucuronidation of steroids and xenobiotics, is a novel, estrogen-regulated gene in estrogen receptor (ER)-positive human breast cancer cells (MCF-7, BT474, T47D, and ZR-75). UGT2B15 is the onl

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Pokrovsky, Vadim S., Olga E. Chepikova, Denis Zh Davydov, Andrey A. Zamyatnin Jr, Alexander N. Lukashev, and Elena V. Lukasheva. "Amino Acid Degrading Enzymes and their Application in Cancer Therapy." Current Medicinal Chemistry 26, no. 3 (2019): 446–64. http://dx.doi.org/10.2174/0929867324666171006132729.

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Background:Amino acids are essential components in various biochemical pathways. The deprivation of certain amino acids is an antimetabolite strategy for the treatment of amino acid-dependent cancers which exploits the compromised metabolism of malignant cells. Several studies have focused on the development and preclinical and clinical evaluation of amino acid degrading enzymes, namely L-asparaginase, L-methionine γ-lyase, L-arginine deiminase, L-lysine α-oxidase. Further research into cancer cell metabolism may therefore define possible targets for controlling tumor growth.Objective:The purp

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