University of California, San Francisco, USA
Posters & Accepted Abstracts: J Cancer Sci Ther
Recently, long non-coding RNAs have emerged as new gene regulators and prognostic markers in several cancers including renal cancer. In this study, we examined the role and effect of long non-coding RNA MALAT1 in renal cell carcinoma (RCC). We looked at MALAT1 expression in renal cancer tissues, cell lines and performed functional analyses to determine its role in RCC. The transcriptional regulation of MALAT1 and its interactions with Ezh2 (Enhancer of zeste homolog 2) (Ezh2) and miR-205 were investigated in RCC cells. This study shows that MALAT1 expression was significantly higher in human renal cancer tissues and was associated with over-all shorter survival. Renal cancer cell proliferation and invasion were significantly decreased and apoptosis was significantly increased by MALAT1 knock down in RCC cells. MALAT1 was transcriptionally activated by c-Fos in RCC cells and shown to interact with Ezh2 by immunoprecipitation. After knock down of MALAT1, E-cadherin expression was increased while beta-catenin expression was decreased through Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed. Our data indicates that MALAT1 plays an important oncogenic function in RCC and its transcriptional activation by c-Fos contributes to increased renal cancer oncogenesis. MALAT1 binds to Ezh2 and after MALAT1 knock down, oncogenesis was inhibited by depletion of Ezh2. This resulted in inhibition of EMT via recovery of E-cadherin and down-regulation of beta-catenin in renal cancer cells. Our results indicate that MALAT1 may be a new therapeutic target and biomarker for renal cancer.
Cancer Science & Therapy received 3644 citations as per Google Scholar report