RETRACTED: MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1 (Retracted Article)

被引:27
作者
Hong, Chun-Fu [1 ]
Lin, Shu-Yu [2 ]
Chou, Yu-Ting [3 ]
Wu, Cheng-Wen [4 ,5 ,6 ,7 ]
机构
[1] Natl Quemoy Univ, Dept Long Term Care, Jinning Township 89250, Kinmen County, Taiwan
[2] Acad Sinica, Inst Biol Chem, Natl Res Program Genom Med Core Facil Prote & Gly, Taipei 11529, Taiwan
[3] Natl Tsing Hua Univ, Inst Biotechnol, Hsinchu 30013, Taiwan
[4] Natl Yang Ming Univ, Inst Clin Med, Taipei 11221, Taiwan
[5] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 11221, Taiwan
[6] Natl Yang Ming Univ, Inst Microbiol & Immunol, Taipei 11221, Taiwan
[7] Acad Sinica, Inst Biomed Sci, Taipei 11221, Taiwan
关键词
LUNG-CANCER; DRUG-RESISTANCE; CLIP-SEQ; CHEMOTHERAPY; COMPLEX; BAF60A; GROWTH; RNAS; CHEMORESISTANCE; ADENOCARCINOMA;
D O I
10.1074/jbc.M115.667568
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We previously demonstrated that the epidermal growth factor receptor (EGFR) up-regulated miR-7 to promote tumor growth during lung cancer oncogenesis. Several lines of evidence have suggested that alterations in chromatin remodeling components contribute to cancer initiation and progression. In this study, we identified SMARCD1 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily d, member 1) as a novel target gene of miR-7. miR-7 expression reduced SMARCD1 protein expression in lung cancer cell lines. We used luciferase reporters carrying wild type or mutated 3'UTR of SMARCD1 and found that miR-7 blocked SMARCD1 expression by binding to two seed regions in the 3'UTR of SMARCD1 and down-regulated SMARCD1 mRNA expression. Additionally, upon chemotherapy drug treatment, miR-7 downregulated p53-dependent apoptosis-related gene BAX (BCL2-associated X protein) and p21 expression by interfering with the interaction between SMARCD1 and p53, thereby reducing caspase3 cleavage and the downstream apoptosis cascades. We found that although SMARCD1 sensitized lung cancer cells to chemotherapy drug-induced apoptosis, miR-7 enhanced the drug resistance potential of lung cancer cells against chemotherapy drugs. SMARCD1 was down-regulated in patients with non-small cell lung cancer and lung adenocarcinoma cell lines, and SMARCD1 and miR-7 expression levels were negatively correlated in clinical samples. Our investigation into the involvement of the EGFR-regulated microRNA pathway in the SWI/SNF chromatin remodeling complex suggests that EGFR-mediated miR-7 suppresses the coupling of the chromatin remodeling factor SMARCD1 with p53, resulting in increased chemo-resistance of lung cancer cells.
引用
收藏
页码:1877 / 1889
页数:13
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