TFAP2C-Activated MALAT1 Modulates the Chemoresistance of Docetaxel-Resistant Lung Adenocarcinoma Cells

被引：56

作者：

Chen, Jing ^{[1
,2
]}

Liu, Xiaobei ^{[2
]}

Xu, Yichen ^{[2
]}

Zhang, Kai ^{[2
]}

Huang, Jiayuan ^{[3
]}

Pan, Banzhou ^{[3
]}

Chen, Dongqin ^{[4
]}

Cui, Shiyun ^{[5
]}

Song, Haizhu ^{[2
]}

Wang, Rui ^{[2
]}

Chu, Xiaoyuan ^{[2
]}

Zhu, Xiaoli ^{[1
]}

Chen, Longbang ^{[2
]}

机构：

[1] Southeast Univ, Zhongda Hosp, Dept Resp, Nanjing, Jiangsu, Peoples R China

[2] Nanjing Univ, Sch Med, Jinling Hosp, Dept Med Oncol, Nanjing 210002, Jiangsu, Peoples R China

[3] Nanjing Med Univ, Jiangsu Inst Canc Res, Jiangsu Canc Hosp, Dept Med Oncol, Nanjing, Jiangsu, Peoples R China

[4] Soochow Univ, Affiliated Hosp 1, Dept Med Oncol, Suzhou, Jiangsu, Peoples R China

[5] Nanjing Med Univ, Affiliated Hosp 1, Dept Med Oncol, Suzhou, Jiangsu, Peoples R China

来源：

MOLECULAR THERAPY NUCLEIC ACIDS | 2019年 / 14卷

基金：

中国国家自然科学基金;

关键词：

LONG NONCODING RNA; CANCER STATISTICS; PROLIFERATION; TUMOR; TRANSCRIPTION; CONTRIBUTES; PROGRESSION; PROMOTE; GROWTH; CERNA;

D O I：

10.1016/j.omtn.2019.01.005

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Chemoresistance remains a great obstacle in effective lung adenocarcinoma (LUAD) treatment. Previously, we verified the role of microRNA-200b (miR-200b) in the formation of docetaxel (DTX)-resistant LUAD cells. This study aims to investigate the mechanism underlying the low level of miR-200b in DTX-resistant LUAD cells. The real-time reverse transcription (RT2) lncRNA PCR array system was applied to explore lncRNAs that potentially regulated miR-200b in DTX-resistant LUAD cells. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) contributed to the low miR-200b level in DTX-resistant LUAD cells. Functional assays were conducted to determine the role of MALAT1 in regulating the growth and metastasis of parental and DTX-resistant LUAD cells. Investigation revealed the mechanism of the competing endogenous RNA (ceRNA) pathway. MALAT1 regulated miR-200b by acting as a ceRNA. MALAT1 modulated the sensitivity of LUAD cells to DTX. E2F transcription factor 3 (E2F3) and zinc-finger E-box binding homeobox 1 (ZEB1) were two targets of miR-200b and mediated the function of MALAT1 in DTX-resistant LUAD cells. Transcription factor AP-2 gamma (TFAP2C) and ZEB1 activated the MALAT1 transcription. In conclusion, TFAP2C-activated MALAT1 modulated the chemoresistance of LUAD cells by sponging miR-200b to upregulate E2F3 and ZEB1. Our findings may provide novel therapeutic targets and perspectives for LUAD treatment.

引用

页码：567 / 582

页数：16

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