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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
by
Wei, Ran
, He, Shujin
, Zhang, Yu
, Wu, Yemeng
, Lu, Xiangtong
, Duan, Jing
, Xiang, Chuqi
, Cai, Zhenyu
, Mei, Renmei
, Xiong, Lixia
, Kang, Yurong
in
A549 Cells
/ Adenocarcinoma - genetics
/ Adenocarcinoma - metabolism
/ Adenocarcinoma of Lung
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Cytokines
/ Epigenetics
/ Fibroblasts
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genetic aspects
/ Humans
/ IL-13
/ Interleukin-13 - pharmacology
/ Interleukins
/ lung adenocarcinoma
/ Lung cancer
/ Lung Neoplasms - genetics
/ Lung Neoplasms - metabolism
/ Medical research
/ MicroRNAs - genetics
/ miR-29a
/ Neoplasm Invasiveness
/ PI3K/AKT pathway
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Risk factors
/ Roles
/ Signal Transduction
/ Smooth muscle
/ Studies
/ Transcription factors
/ Tumorigenesis
/ Tumors
/ YY1
/ YY1 Transcription Factor - genetics
/ YY1 Transcription Factor - metabolism
2018
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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
by
Wei, Ran
, He, Shujin
, Zhang, Yu
, Wu, Yemeng
, Lu, Xiangtong
, Duan, Jing
, Xiang, Chuqi
, Cai, Zhenyu
, Mei, Renmei
, Xiong, Lixia
, Kang, Yurong
in
A549 Cells
/ Adenocarcinoma - genetics
/ Adenocarcinoma - metabolism
/ Adenocarcinoma of Lung
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Cytokines
/ Epigenetics
/ Fibroblasts
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genetic aspects
/ Humans
/ IL-13
/ Interleukin-13 - pharmacology
/ Interleukins
/ lung adenocarcinoma
/ Lung cancer
/ Lung Neoplasms - genetics
/ Lung Neoplasms - metabolism
/ Medical research
/ MicroRNAs - genetics
/ miR-29a
/ Neoplasm Invasiveness
/ PI3K/AKT pathway
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Risk factors
/ Roles
/ Signal Transduction
/ Smooth muscle
/ Studies
/ Transcription factors
/ Tumorigenesis
/ Tumors
/ YY1
/ YY1 Transcription Factor - genetics
/ YY1 Transcription Factor - metabolism
2018
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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
by
Wei, Ran
, He, Shujin
, Zhang, Yu
, Wu, Yemeng
, Lu, Xiangtong
, Duan, Jing
, Xiang, Chuqi
, Cai, Zhenyu
, Mei, Renmei
, Xiong, Lixia
, Kang, Yurong
in
A549 Cells
/ Adenocarcinoma - genetics
/ Adenocarcinoma - metabolism
/ Adenocarcinoma of Lung
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Cytokines
/ Epigenetics
/ Fibroblasts
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genetic aspects
/ Humans
/ IL-13
/ Interleukin-13 - pharmacology
/ Interleukins
/ lung adenocarcinoma
/ Lung cancer
/ Lung Neoplasms - genetics
/ Lung Neoplasms - metabolism
/ Medical research
/ MicroRNAs - genetics
/ miR-29a
/ Neoplasm Invasiveness
/ PI3K/AKT pathway
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Risk factors
/ Roles
/ Signal Transduction
/ Smooth muscle
/ Studies
/ Transcription factors
/ Tumorigenesis
/ Tumors
/ YY1
/ YY1 Transcription Factor - genetics
/ YY1 Transcription Factor - metabolism
2018
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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
Journal Article
miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
2018
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Overview
IL-13 is a proinflammatory cytokine associated with multiple pathological conditions and the promotion of metastasis in lung cancer. Previous studies have demonstrated that IL-13 and YY1 are associated with PI3K/AKT signaling. In addition, miR-29a has been found to play a critical role in cell invasion in lung cancer. However, the molecular mechanism of miR-29a underlying its involvement in IL-13-induced lung cancer cell invasion remains largely unknown. In the present study, we aimed to investigate the role of miR-29a in cell invasion mediated by IL-13 in lung cancer. By using MTT and wound-scratch assays, we assessed cell proliferation and migration induced by IL-13, and identified activation of the PI3K/AKT/YY1 pathway. Inhibition of PI3K/AKT by LY294002 downregulated IL-13-induced YY1 expression. Furthermore, we found that miR-29a directly targets YY1 and suppressed its expression in lung cancer. By using MTT, flow cytometry and Transwell assays, overexpression of miR-29a restricted both YY1 and N-cadherin expression, and inhibited IL-13-induced invasion of lung cancer A549 cells. Taken together, these findings demonstrate that PI3K/AKT/YY1 is involved in the regulation of lung cancer cell behavior induced by IL-13, and miR-29a represents a promising therapeutic target.
Publisher
D.A. Spandidos,Spandidos Publications,Spandidos Publications UK Ltd
Subject
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Humans
/ IL-13
/ Interleukin-13 - pharmacology
/ miR-29a
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Roles
/ Studies
/ Tumors
/ YY1
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