Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
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Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Τρίτη 16 Μαΐου 2017

miR-133 involves in lung adenocarcinoma cell metastasis by targeting FLOT2.

miR-133 involves in lung adenocarcinoma cell metastasis by targeting FLOT2.

Artif Cells Nanomed Biotechnol. 2017 May 14;:1-7

Authors: Wei G, Xu Y, Peng T, Yan J

Abstract
BACKGROUND: Dysregulated microRNAs (miRNAs) reported to involve into the oncogenesis and progression in various human cancers. However, the roles and mechanism of miR-133 in lung adenocarcinoma remain largely unclear.
METHODS: In this study, qPCR assay and western blot were used to detect the expression levels of miR-133, Akt and FLOT2. Luciferase reporter assay was used to identify the target role of miR-133 on FLOT2. The cell invasion and the migration capability were performed using the transwell invasion assay and wound healing assay.
RESULTS: We found that miR-133 expression levels were downregulated in human lung adenocarcinoma specimens and cell lines compared with the adjacent normal tissues and normal human bronchial epithelial cell. miR-133 significantly suppressed metastasis of lung adenocarcinoma cells in vitro. Furthermore, FLOT2 (flotillin-2) identified as a direct target of miR-133, and FLOT2 expression levels were inversely correlated with miR-133 expression levels in human lung adenocarcinoma specimens. And the restoration studies suggested FGF2 as a downstream effector of miR-133 which acted through Akt signalling pathway.
CONCLUSIONS: Our study revealed the mechanism that miR-133 suppresses lung adenocarcinoma metastasis by targeting FLOT2 via Akt signalling pathway, implicating a potential prognostic biomarker and therapeutic target for lung adenocarcinoma treatment.

PMID: 28503944 [PubMed - as supplied by publisher]



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