Zhou Yingchen, Zhang Yang, Li Weiqing, Xu Jinming, He Xia, Li Xianxin, Wang Yan
Department of Surgery, Fuwai Hospital Chinese Academic of Medical Science Shenzhen, The University of South China, Shenzhen, People's Republic of China.
Department of Urology, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, People's Republic of China.
Cancer Manag Res. 2020 Oct 2;12:9589-9597. doi: 10.2147/CMAR.S271647. eCollection 2020.
Renal cell carcinoma (RCC) is one of the most common tumors in urinary tract tumors. However, the mechanism that supports renal cell carcinoma is unclear. The function of transcription elongation factor A (SII)-like 2 (TCEAL2) and its association with human cancer have not been reported.
To explore the role of TCEAL2 in carcinogenesis of clear cell renal cell carcinoma (ccRCC), we performed bioinformatics analysis to determine the expression levels of TCEAL2 in ccRCC specimens and normal kidney tissue and then verified findings with our samples by qPCR, Western blot and immunohistochemistry staining. Furthermore, the lentiviral vectors were used to increase the expression of TCEAL2 in ccRCC cell lines. The immunofluorescence assay was taken to observe the subcellular location of TCEAL2 in ccRCC cells, and CCK-8 and flow cytometry were introduced for assessing cell proliferation and cell cycle of ccRCC cells, respectively.
Compared with adjacent normal kidney tissue and human proximal tubular epithelial cells, the expression of TCEAL2 in ccRCC tissues and cell lines was down-regulated. Patients who had low expression of TCEAL2 had a statistically significant late tumor stage. Restore of TCEAL2 in ccRCC cells inhibited cell proliferation and induced cell cycle arrest in S phase of ccRCC cells.
To our knowledge, this is the first report of TCEAL2 expression changes in ccRCC. We found that the decrease of TCEAL2 expression may be related to the occurrence of ccRCC. Further research is needed to clarify the molecular mechanism of TCEAL2 in progress of ccRCC.
肾细胞癌（RCC）是泌尿系统肿瘤中最常见的肿瘤之一。然而，支持肾细胞癌发生的机制尚不清楚。转录延伸因子A（SII）样2（TCEAL2）的功能及其与人类癌症的关系尚未见报道。
为探讨TCEAL2在透明细胞肾细胞癌（ccRCC）发生中的作用，我们进行了生物信息学分析以确定TCEAL2在ccRCC标本和正常肾组织中的表达水平，然后通过qPCR、蛋白质免疫印迹和免疫组织化学染色用我们的样本验证结果。此外，使用慢病毒载体增加ccRCC细胞系中TCEAL2的表达。采用免疫荧光测定法观察TCEAL2在ccRCC细胞中的亚细胞定位，并分别引入CCK-8和流式细胞术评估ccRCC细胞的增殖和细胞周期。
与相邻正常肾组织和人近端肾小管上皮细胞相比，ccRCC组织和细胞系中TCEAL2的表达下调。TCEAL2低表达的患者肿瘤分期较晚，差异具有统计学意义。ccRCC细胞中TCEAL2的恢复抑制了细胞增殖并诱导ccRCC细胞在S期发生细胞周期阻滞。
据我们所知，这是关于ccRCC中TCEAL2表达变化的首次报道。我们发现TCEAL2表达的降低可能与ccRCC的发生有关。需要进一步研究以阐明TCEAL2在ccRCC进展中的分子机制。
