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ATAD2通过调节c-Myc的转录活性促进透明细胞肾细胞癌的糖酵解和肿瘤进展。

ATAD2 promotes glycolysis and tumor progression in clear cell renal cell carcinoma by regulating the transcriptional activity of c-Myc.

作者信息

Wu Zonglong, Ge Liyuan, Song Yimeng, Deng Shaohui, Duan Peichen, Du Tan, Wu Yaqian, Zhang Zhanyi, Hou Xiaofei, Ma Lulin, Zhang Shudong

机构信息

Department of Urology, Peking University Third Hospital, Beijing, 100191, P.R. China.

出版信息

Discov Oncol. 2023 May 26;14(1):79. doi: 10.1007/s12672-023-00696-1.

Abstract

Clear cell renal cell carcinoma (ccRCC) is a common malignant tumor of the urogenital tract. Given that ccRCC is often resistant to radiotherapy and traditional chemotherapy, the clinical treatment of patients with ccRCC remains a challenge. The present study found that ATAD2 was significantly upregulated in ccRCC tissues. In vitro and in vivo experiments showed that the inhibition of ATAD2 expression mitigated the aggressive phenotype of ccRCC. ATAD2 was also associated with glycolysis in ccRCC. Interestingly, we found that ATAD2 could physically interact with c-Myc and promote the expression of its downstream target gene, thereby enhancing the Warburg effect of ccRCC. Overall, our study emphasizes the role of ATAD2 in ccRCC. The targeted expression or functional regulation of ATAD2 could be a promising method to reduce the proliferation and progression of ccRCC.

摘要

透明细胞肾细胞癌(ccRCC)是泌尿生殖道常见的恶性肿瘤。鉴于ccRCC通常对放疗和传统化疗耐药,ccRCC患者的临床治疗仍然是一项挑战。本研究发现,ATAD2在ccRCC组织中显著上调。体外和体内实验表明,抑制ATAD2表达可减轻ccRCC的侵袭性表型。ATAD2还与ccRCC中的糖酵解有关。有趣的是,我们发现ATAD2可与c-Myc发生物理相互作用并促进其下游靶基因的表达,从而增强ccRCC的瓦氏效应。总体而言,我们的研究强调了ATAD2在ccRCC中的作用。靶向ATAD2的表达或功能调控可能是减少ccRCC增殖和进展的一种有前景的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3585/10219916/7cda11c95175/12672_2023_696_Fig1_HTML.jpg

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