No abstract

BackgroundC-MYC, LIN28, OCT4, KLF4, NANOG and SOX2 are stem cell related factors. We detected whether these factors express in renal cell carcinoma (RCC) tissues to study their correlations with the clinical and pathological characteristics.MethodsThe expressions of c-MYC, LIN28, SOX2, KLF4, OCT4 and NANOG in 30 RCC patients and 5 non-RCC patients were detected with quantitative real-time reverse transcription-PCR (qRT-PCR). The data were analyzed with Wilcoxon signed rank sum test and x2 test.ResultsIn RCC group, c-MYC expression was significantly higher in RCC tissues compared with normal tissues (P < 0.05). The expression levels of OCT4, KLF4, NANOG and SOX2 were significantly lower in RCC tissues compared with normal tissues (P < 0.05). LIN28 expression level was not significant. No difference was observed when it comes to clinical and pathological characteristics such as gender, age, tumor size, cTNM classification and differentiation status (P > 0.05). Also the expression levels of all above factors were not significantly changed in non-RCC group (P > 0.05).ConclusionsThe present analysis strongly suggests that altered expression of several stem cell related factors may play different roles in RCC. C-MYC may function as an oncogene and OCT4, KLF4, NANOG and SOX2 as tumor suppressors.

Reduced expression of FOXO1 is common in RCC and a potentially suitable marker of different histological subtypes and prognosis of cRCC. Increasing expression of FOXO1 by the miR-27a inhibitor could prevent cell growth.

MicroRNA-34a (miR-34a) is a tumor suppressive microRNA, which induces G1 arrest, apoptosis and senescence by repressing the expression of multiple oncogenes. This study aimed to investigate the biological function and molecular mechanisms of miR-34a in human renal cell carcinoma (RCC) cells. Quantitative polymerase chain reaction (qPCR) revealed that miR-34a expression was significantly downregulated in eight of the 10 (80%) RCC tissues compared with adjacent normal tissues. In RCC cell lines, several other target genes of miR-34a were dysregulated at the mRNA level when the expression of miR-34a was elevated. In addition, western blot analysis and qPCR revealed that forced expression of miR-34a downregulated the expression of Notch1 at the protein and mRNA level. The Cell Counting Kit-8 identified that transient forced expression of miR-34a inhibited cell growth and resulted in cell cycle arrest, which was evaluated by flow cytometry. Our data demonstrated that miR-34a inhibits cell proliferation by downregulating Notch1 in RCC cell lines.

The pathogenesis of ulcerative colitis in rats involves abnormality of apoptosis. Acupuncture and moxibustion can regulate the expression of Bcl-2, Bax, fas and FasL proteins and inhibit the apoptosis of epithelial cells of ulcerative colitis in rats by Bcl-2/Bax, fas/FasL pathways.