Open AccessMiR‐130b promotes the progression of oesophageal squamous cell carcinoma by targeting SASH 1
Author(s) -
Zhu Yuxing,
Ma Yanni,
Peng Honghua,
Gong Lian,
Xiao Mengqin,
Xiang Liang,
He Dong,
Cao Ke
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13887
Subject(s) - flow cytometry , in vivo , western blot , cell culture , microbiology and biotechnology , cell , cell growth , reporter gene , apoptosis , biology , cancer research , gene , gene expression , biochemistry , genetics
MiR‐130b and SAM and SH 3 domain containing 1 ( SASH 1 ) play an important role in many types of human cancers. The aim of our research was to study their interactions in the process of the proliferation and aggressiveness of oesophageal squamous cell carcinoma ( ESCC ) cells. Microarray analysis was done to screen the differentially expressed genes in the ESCC tissues. miR‐130b and SASH 1 mRNA levels in the ESCC tissues and cells were detected by qRT ‐ PCR . Dual luciferase reporter system was used to verify the target relationship between miR‐130b and SASH 1 . The effects of miR‐130b on SASH 1 expression were explored by western blot in KYSE 30 and TE 1 cell lines. CCK ‐8 assay, flow cytometry, Transwell, and wound healing assays were conducted to explore the effects of miR‐130b and SASH 1 in vitro. In addition, in vivo experiments were conducted to study the roles of miR‐130b and SASH 1 . miR‐130b was highly expressed, while SASH 1 was the opposite in both the ESCC tissues and cells. The expression of SASH 1 was inhibited by the direct binding of miR‐130b. The inhibition of miR‐130b reduced the proliferation and aggressiveness of ESCC cells, while it also induced apoptosis and cell cycle arrest in the ESCC cells by suppressing SASH 1 . The in vivo assay suggested that the overexpression of miR‐130b promoted the growth of ESCC tumours. MiR‐130b was up‐regulated in the ESCC tumour tissues and cells, acting as a tumour promoter. A stimulating effect was demonstrated on ESCC cell growth and aggressiveness by suppressing SASH 1, which is an anti‐oncogene.