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Dual role of G-quadruplex in translocation renal cell carcinoma: Exploring plausible Cancer therapeutic innovation.
Biochimica et Biophysica Acta (BBA) - General Subjects ( IF 3 ) Pub Date : 2020-08-31 , DOI: 10.1016/j.bbagen.2020.129719
Neha 1 , Parimal Das 1 , Shiv Prakash Verma 2
Affiliation  

Background

Renal Cell Carcinoma (RCC) is the ninth leading cause of death among kidney cancer. Xp11.2 translocation harboring TFE3 fusion proteins, act as an oncogene in translocation cancers that constitute the hallmark of translocation renal cell carcinoma (tRCC). G-quadruplex (G4), an alternative nucleic acid structure is an emerging and promising factor in cancer. The presence of G4 within the genome plays a pioneering role in cancer as it contributes to genomic aberration as well as inhibition in cell proliferation.

Scope of review

Here we discuss the link between G4 and tRCC. We compile the available information of G-quadruplex & propose their dual role in tRCC, suggesting both stabilization and destabilization of G-quadruplex could be considered targets for tRCC.

Major conclusions

Our in Silico analysis of TFE3 and their three fusions partner's PRCC, SFPQ, and ASPSCR1 discloses a few putative G4 forming sequences (PQS) in their corresponding fusion gene or fusion transcript. Stabilization of G4 structure within fusion gene/transcript can be of great use towards potential therapeutics targeting fusion protein derived oncogenesis, as G4 is a serious menace for DNA polymerization, transcription & translation. G-quadruplex at intron-2 of the TFE3 has been reported to mediate its translocation also. Both stabilization and destabilization of the G4 structure would be a promising approach in the suppression of cancerous cell proliferation.

General significance

Pioneering studies discovered the relevance of G4 in cancer therapy and explore our approaches towards therapeutic innovation against oncogenic fusion protein and tRCC. Selectively targeting G4 in oncogenic fusion transcript will emerge as potential druggable structures.



中文翻译:

G四联体在易位性肾细胞癌中的双重作用:探索可能的癌症治疗创新。

背景

肾细胞癌(RCC)是肾癌中第九大死亡原因。Xp11.2易位包含TFE3融合蛋白,在易位癌中起癌基因的作用,易位癌构成易位肾细胞癌(tRCC)的标志。G-四链体(G4),一种替代的核酸结构,是癌症中一个新兴且有希望的因素。基因组中G4的存在在癌症中起着先锋作用,因为它有助于基因组畸变以及抑制细胞增殖。

审查范围

在这里,我们讨论G4和tRCC之间的联系。我们汇总了G-四链体的可用信息并提出了它们在tRCC中的双重作用,这表明G-四链体的稳定和去稳定都可以视为tRCC的目标。

主要结论

我们对TFE3及其三个融合伙伴的PRCCSFPQASPSCR1的in silico分析揭示了在其相应的融合基因或融合转录本中一些推定的G4形成序列(PQS)。融合基因/转录本中G4结构的稳定化对于靶向融合蛋白衍生的肿瘤发生的潜在治疗方法可能非常有用,因为G4是DNA聚合,转录和翻译的严重威胁。据报道,TFE3内含子2的G四联体也介导其易位。G4结构的稳定和去稳定化都是抑制癌细胞增殖的有前途的方法。

一般意义

开拓性研究发现了G4在癌症治疗中的相关性,并探索了我们针对致癌融合蛋白和tRCC进行治疗创新的方法。在致癌融合转录物中选择性靶向G4将作为潜在的可药物化结构出现。

更新日期:2020-09-08
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