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2015 ; 5
(ä): 15972
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Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing
Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma
#MMPMID26522444
Zhou X
; Liu S
; Cai G
; Kong L
; Zhang T
; Ren Y
; Wu Y
; Mei M
; Zhang L
; Wang X
Sci Rep
2015[Nov]; 5
(ä): 15972
PMID26522444
show ga
The prognosis of advanced oral squamous cell carcinoma (OSCC) patients remains
dismal, and a better understanding of the underlying mechanisms is critical for
identifying effective targets with therapeutic potential to improve the survival
of patients with OSCC. This study aims to clarify the clinical and biological
significance of metastasis-associated long non-coding RNA, metastasis-associated
lung adenocarcinoma transcript 1 (MALAT1) in OSCC. We found that MALAT1 is
overexpressed in OSCC tissues compared to normal oral mucosa by real-time PCR.
MALAT1 served as a new prognostic factor in OSCC patients. When knockdown by
small interfering RNA (siRNA) in OSCC cell lines TSCCA and Tca8113, MALAT1 was
shown to be required for maintaining epithelial-mesenchymal transition (EMT)
mediated cell migration and invasion. Western blot and immunofluorescence
staining showed that MALAT1 knockdown significantly suppressed N-cadherin and
Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both
nucleus and cytoplasm levels of ?-catenin and NF-?B were attenuated, while
elevated MALAT1 level triggered the expression of ?-catenin and NF-?B. More
importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth
in vivo. Therefore, these findings provide mechanistic insight into the role of
MALAT1 in regulating OSCC metastasis, suggesting that MALAT1 is an important
prognostic factor and therapeutic target for OSCC.