hADA3和HPVE6致癌伙伴关系的机制见解-为改善宫颈癌治疗铺平道路

IF 1.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

高危人乳头瘤病毒(HPV)被认为是宫颈癌的主要病原体,宫颈癌是一种发病率很高的毁灭性疾病。在印度,子宫颈癌是妇女癌症死亡的主要原因之一。这种疾病的治疗效果不佳是一个令人严重关切的问题,因此需要积极的研究努力,以发现更有效的治疗方法。在分子水平上了解HPV癌变的复杂性可以促进有希望的抗病毒药物的发现。我们的研究旨在通过揭示一些有助于HPV致癌的关键分子机制来满足时代的需要,这些机制可以用来发现有前途的抗癌分子。我们描述了hADA3和HPVE6之间的致癌联系,并说明了它在细胞转化中的关键作用。我们的工作还显示了HPV癌蛋白如何利用细胞SUMO机制下调hADA3以诱导恶性肿瘤。这激发了我们确定hADA3-E6相互作用的热点,并设计针对HPV诱导的宫颈癌的治疗肽。现就HPV发病机制的研究进展及其对改进宫颈癌治疗方法的启示作一综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanistic insights into the oncogenic partnership of hADA3 and HPVE6 - paving ways for improved cervical cancer therapy
High risk Human Papillomavirus (HPV) is considered the primary causative agent of cervical cancer, a devastating malady with significant morbidity. In India, cervical cancer is one of the major reasons of cancer mortality among women. Poor treatment outcomes of this disease is a matter of grave concern and hence demands aggressive research efforts towards discovery of more effective therapies. Understanding the intricacies of HPV oncogenesis at the molecular level can facilitate the discovery of promising anti-viral drugs. Our research aims at catering to the need of the time by revealing some of the key molecular mechanisms that contributes to HPV oncogenesis that can be utilized to discover promising anti-cancer molecules. We delineated the oncogenic connections between hADA3 and HPVE6 and illustrated its critical role in cellular transformation. Our work also shows how HPV oncoproteins exploits the cellular SUMO machinery to downregulate hADA3 to induce malignancy. This intrigued us to identify the hot spots of hADA3-E6 interaction and design therapeutic peptides against HPV induced cervical cancer. Present review is an attempt to outline our research on novel mechanisms of HPV pathogenesis and its implication on development of improved cervical cancer therapies.
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来源期刊
Indian journal of biochemistry & biophysics
Indian journal of biochemistry & biophysics 生物-生化与分子生物学
CiteScore
2.90
自引率
50.00%
发文量
88
审稿时长
3 months
期刊介绍: Started in 1964, this journal publishes original research articles in the following areas: structure-function relationships of biomolecules; biomolecular recognition, protein-protein and protein-DNA interactions; gene-cloning, genetic engineering, genome analysis, gene targeting, gene expression, vectors, gene therapy; drug targeting, drug design; molecular basis of genetic diseases; conformational studies, computer simulation, novel DNA structures and their biological implications, protein folding; enzymes structure, catalytic mechanisms, regulation; membrane biochemistry, transport, ion channels, signal transduction, cell-cell communication, glycobiology; receptors, antigen-antibody binding, neurochemistry, ageing, apoptosis, cell cycle control; hormones, growth factors; oncogenes, host-virus interactions, viral assembly and structure; intermediary metabolism, molecular basis of disease processes, vitamins, coenzymes, carrier proteins, toxicology; plant and microbial biochemistry; surface forces, micelles and microemulsions, colloids, electrical phenomena, etc. in biological systems. Solicited peer reviewed articles on contemporary Themes and Methods in Biochemistry and Biophysics form an important feature of IJBB. Review articles on a current topic in the above fields are also considered. They must dwell more on research work done during the last couple of years in the field and authors should integrate their own work with that of others with acumen and authenticity, mere compilation of references by a third party is discouraged. While IJBB strongly promotes innovative novel research works for publication as full length papers, it also considers research data emanating from limited objectives, and extension of ongoing experimental works as ‘Notes’. IJBB follows “Double Blind Review process” where author names, affiliations and other correspondence details are removed to ensure fare evaluation. At the same time, reviewer names are not disclosed to authors.
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