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2015 ; 75
(7
): 1322-31
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Long Noncoding RNA MALAT1 Promotes Aggressive Renal Cell Carcinoma through Ezh2
and Interacts with miR-205
#MMPMID25600645
Hirata H
; Hinoda Y
; Shahryari V
; Deng G
; Nakajima K
; Tabatabai ZL
; Ishii N
; Dahiya R
Cancer Res
2015[Apr]; 75
(7
): 1322-31
PMID25600645
show ga
Recently, long noncoding RNAs (lncRNA) have emerged as new gene regulators and
prognostic markers in several cancers, including renal cell carcinoma (RCC). In
this study, we investigated the contributions of the lncRNA MALAT1 in RCC with a
specific focus on its transcriptional regulation and its interactions with Ezh2
and miR-205. We found that MALAT1 expression was higher in human RCC tissues,
where it was associated with reduced patient survival. MALAT1 silencing decreased
RCC cell proliferation and invasion and increased apoptosis. Mechanistic
investigations showed that MALAT1 was transcriptionally activated by c-Fos and
that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was
increased, whereas ?-catenin expression was decreased through Ezh2. Reciprocal
interaction between MALAT1 and miR-205 was also observed. Lastly, MALAT1 bound
Ezh2 and oncogenesis facilitated by MALAT1 was inhibited by Ezh2 depletion,
thereby blocking epithelial-mesenchymal transition via E-cadherin recovery and
?-catenin downregulation. Overall, our findings illuminate how overexpression of
MALAT1 confers an oncogenic function in RCC that may offer a novel theranostic
marker in this disease.
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