Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis
Background Non‐small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further unde...
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doaj-997467ca0b204ef09715665ce70f3efa2020-11-24T22:57:44ZengWileyThoracic Cancer1759-77061759-77142020-02-0111226427610.1111/1759-7714.13245Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axisLingling Pang0Yun Cheng1Shenchun Zou2Jie Song3Department of Respiratory Medicine Yantai Yuhuangding Hospital Yantai ChinaDepartment of Respiratory Medicine Yantai Muping District Traditional Chinese Medical Hospital Yantai ChinaDepartment of Respiratory Medicine Yantai Yuhuangding Hospital Yantai ChinaDepartment of Respiratory Medicine Yantai Yuhuangding Hospital Yantai ChinaBackground Non‐small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further understanding. Methods The expression of SNHG7, miR‐449a and TGIF2 in NSCLC tumors and cells was examined by quantitative real time polymerase chain reaction (qRT‐PCR). Cell viability was measured by MTT assay. Cell migration and invasion was conducted using transwell assay. Protein expression of TGIF2, vimentin, N‐cadherin and E‐cadherin was detected by western blot. The interaction between miR‐449a and SNHG7 or TGIF2 was determined by luciferase reporter system, RIP and RNA pull‐down assay, respectively. Xenograft mice models were established by subcutaneously injecting A549 cells transfected with sh‐SNHG7 and sh‐control. Results SNHG7 expression was upregulated in NSCLC tumors and cells compared with normal tissues and cells. SNHG7 silencing repressed cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) in NSCLC. Consistently, SNHG7 knockdown hindered tumor growth in vivo. The subsequent luciferase reporter system, RIP and RNA pull‐down assay validated the interaction between miR‐449a and SNHG7 or TGIF2. The rescue experiments displayed that miR‐449a inhibitor counteracted SNHG7 silencing induced inhibition on proliferation, migration, invasion and EMT. Similarly, restoration of TGIF2 reversed miR‐449a mediated inhibition on cell progression. In addition, the results indicated that SNHG7 could regulate cell progression by targeting miR‐449a/TGIF2 axis. Conclusion SNHG7 contributed to cell proliferation, migration, invasion and EMT in NSCLC by upregulating TGIF2 via sponging miR‐449a, representing a novel targeted therapy method for NSCLC.https://doi.org/10.1111/1759-7714.13245miR‐449aNSCLCprogressionSNHG7TGIF2 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lingling Pang Yun Cheng Shenchun Zou Jie Song |
spellingShingle |
Lingling Pang Yun Cheng Shenchun Zou Jie Song Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis Thoracic Cancer miR‐449a NSCLC progression SNHG7 TGIF2 |
author_facet |
Lingling Pang Yun Cheng Shenchun Zou Jie Song |
author_sort |
Lingling Pang |
title |
Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis |
title_short |
Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis |
title_full |
Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis |
title_fullStr |
Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis |
title_full_unstemmed |
Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis |
title_sort |
long noncoding rna snhg7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating mir‐449a/tgif2 axis |
publisher |
Wiley |
series |
Thoracic Cancer |
issn |
1759-7706 1759-7714 |
publishDate |
2020-02-01 |
description |
Background Non‐small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further understanding. Methods The expression of SNHG7, miR‐449a and TGIF2 in NSCLC tumors and cells was examined by quantitative real time polymerase chain reaction (qRT‐PCR). Cell viability was measured by MTT assay. Cell migration and invasion was conducted using transwell assay. Protein expression of TGIF2, vimentin, N‐cadherin and E‐cadherin was detected by western blot. The interaction between miR‐449a and SNHG7 or TGIF2 was determined by luciferase reporter system, RIP and RNA pull‐down assay, respectively. Xenograft mice models were established by subcutaneously injecting A549 cells transfected with sh‐SNHG7 and sh‐control. Results SNHG7 expression was upregulated in NSCLC tumors and cells compared with normal tissues and cells. SNHG7 silencing repressed cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) in NSCLC. Consistently, SNHG7 knockdown hindered tumor growth in vivo. The subsequent luciferase reporter system, RIP and RNA pull‐down assay validated the interaction between miR‐449a and SNHG7 or TGIF2. The rescue experiments displayed that miR‐449a inhibitor counteracted SNHG7 silencing induced inhibition on proliferation, migration, invasion and EMT. Similarly, restoration of TGIF2 reversed miR‐449a mediated inhibition on cell progression. In addition, the results indicated that SNHG7 could regulate cell progression by targeting miR‐449a/TGIF2 axis. Conclusion SNHG7 contributed to cell proliferation, migration, invasion and EMT in NSCLC by upregulating TGIF2 via sponging miR‐449a, representing a novel targeted therapy method for NSCLC. |
topic |
miR‐449a NSCLC progression SNHG7 TGIF2 |
url |
https://doi.org/10.1111/1759-7714.13245 |
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