Noncoding-RNA mediated high expression of zinc finger protein 268 suppresses clear cell renal cell carcinoma progression by promoting apoptosis and regulating immune cell infiltration

Bioengineered

Yongzhe Gu¹  Weipu Mao²  Yidi Wang³  Xianchao Sun³  Keyi Wang³  Houliang Zhang³  Tianyuan Xu³  Yifan Zhang³  Bo Peng³  Jinliang Ni⁴ 

[1] Department of Neurology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, Zha Bei Qu, China;Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nanjing, Jiangsu, China;Department of Urology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, Zha Bei Qu, China;Shanghai Clinical College, Anhui Medical University, Hefei, Anhui Province, China;

关键词: ZNF268;    kidney renal clear cell carcinoma;    prognosis;    immune infiltration;    noncoding RNA;   

DOI  :  10.1080/21655979.2022.2060787

来源: DOAJ

【 摘 要 】

Clear cell renal cell carcinoma (ccRCC) is one of the most common malignant kidney tumors with a poor prognosis. Accumulating evidence proves that zinc finger protein 268 (ZNF268) is associated with tumor progression, but the detailed regulatory functions of ZNF268 in ccRCC require further exploration. Thus, here we aim to characterize the role of ZNF268 in ccRCC. The clinical significance of ZNF268 was evaluated using The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. Subsequently, tumor-infiltrating immune cells, as well as upstream noncoding RNAs (ncRNAs) related to the tumor-suppressing function of ZNF268, were identified by in silico analyses. The expression of ZNF268 was significantly decreased in ccRCC samples compared with adjacent normal tissues. In addition, ZNF268 expression was negatively correlated with tumor progression and positively correlated with overall and disease-specific survival. TCGA and GTEx databases proved the potential tumor-suppressing function, which was measured both in vitro and in vivo after ZNF268 over-expression. Overexpression of ZNF268 effectively inhibited the proliferation, migration, invasion and promotied apoptosis of the Caki-1. The level of ZNF268 was positively related to the immune cell infiltration in the tumor. Moreover, we determined that the AC093157.1/miR-27a-3p axis can potentially regulate ZNF268 function in ccRCC. Our work describes a novel ncRNA-mediated ZNF268 function in ccRCC. ZNF268 acts as a tumor suppressor, and it is associated with apoptosis and immune cell infiltration in ccRCC.

【 授权许可】

Unknown