Med Oncol 2013,
PMID: 23292834
Sun, Jian; Chen, Zhaoli; Tan, Xiaogang; Zhou, Fang; Tan, Fengwei; Gao, Yibo; Sun, Nan; Xu, Xiaohui; Shao, Kang; He, Jie
Recently, microRNA-99 family members, such as miR-99a/b and miR-100, have been reported to exhibit abnormal expression in various malignant tumors, but their functions in carcinomas are controversial. In this study, we focused on miR-99a and miR-100, which were determined to be universally downregulated in esophageal squamous cell carcinoma, and investigated their functions and potential mechanisms of action. The downregulation of miR-99a/100 was validated by qRT-PCR in 101 ESCC surgical tissue samples and in 3 ESCC cell lines. The overexpression of miR-99a and miR-100 via the transient transfection of the corresponding precursor molecules inhibited cell proliferation by inducing apoptosis in the ESCC cell lines. To investigate the molecular mechanism of miR-99a/100-induced apoptosis, luciferase reporter assays and Western blots were performed to demonstrate that the overexpression of miR-99a/100 suppressed the expression of mTOR by directly targeting its 3'UTR in a post-transcriptional manner. Clinically, the decreased expression of miR-99a/100 was associated with worse overall survival in ESCC patients. In conclusion, these results indicated that miR-99a and miR-100 inhibited cell proliferation by suppressing mTOR in ESCC cell lines, and therefore, the miR-99a/100-mTOR signaling pathway is a potential therapeutic target for inducing apoptosis to combat ESCC.
Diseases/Pathways annotated by Medline MESH: Carcinoma, Squamous Cell, Esophageal Neoplasms
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Text Mining Data
mTOR → miR-99a/100: "
To investigate the molecular mechanism of miR-99a/100 induced apoptosis, luciferase reporter assays and Western blots were performed to demonstrate that the overexpression of
miR-99a/100 suppressed the expression of
mTOR by directly targeting its 3'UTR in a post-transcriptional manner
"
Manually curated Databases
No curated data.