LncRNA TMEM147-AS1/miR-133b/ZNF587 axis regulates Warburg effect and promotes prostatic carcinoma invasion and proliferation

Background: Warburg effect is a characteristic tumor cell behavior regarded as one of the Cancer hallmarks and promotes tumor progression by promoting glucose uptake and lactate production. Long non-coding RNAs (lncRNAs) had been reported to emerge as a vital function in Cancer development. The present research is designed to investigate the underlying molecular mechanism of lncRNA TMEM147 antisense RNA 1 (TMEM147-AS1) on aerobic glycolysis in prostatic carcinoma.

Method: LncRNA TMEM147-AS1, miR-133b, and ZNF587 levels in prostatic carcinoma tissues and cells were detected by PCR or Western blot assays. Cell viability or invasion was determined by Edu, MTT, or Transwell assays. Hematoxylin and eosin (HE) and immunohistochemical (IHC) staining were applied for histopathological examination. Tumor xenograft model was employed to investigate tumor growth in vivo. The combinative relationship between TMEM147-AS1 or ZNF587 and miR-133b was confirmed by luciferase reporter assay.

Result: TMEM147-AS1 and ZNF587 were up-regulated in prostatic carcinoma tissues and cells. Knockdown of TMEM147-AS1 or ZNF587 within prostate Cancer cells significantly restrained cell viability, invasion, and aerobic glycolysis in vitro and suppressed the neoplasia of prostatic carcinoma in vivo. miR-133b was directly targeted in both TMEM147-AS1 and ZNF587. Overexpression of miR-133b restrained prostate Cancer cells' viability, invasion, and aerobic glycolysis. TMEM147-AS1 competitively targeted miR-133b, therefore counteracting miR-133b-mediated repression on ZNF587.

Conclusion: TMEM147-AS1 plays a tumor-promoting action in prostatic carcinoma aerobic glycolysis via affecting the miR-133b/ZNF587 axis, therefore regulating prostatic carcinoma cells invasion and proliferation. These outcomes implied that TMEM147-AS1 could be an effective treatment strategy for further study of prostatic carcinoma.