Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis
Gastric cancer (GC) is a common cancer with high incidence. Understanding the epidemiology and physiopathology of GC is crucial for formulating novel therapeutic strategies. Recent studies have implicated long non-coding RNA LINC00240, miR-338-5p and methyltransferase-like 3 (METTL3) in the progress...
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2021
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oai:doaj.org-article:738da1b18bb240f89e1c42390a1526a92021-12-01T14:41:00ZLong non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis2165-59792165-598710.1080/21655979.2021.1983276https://doaj.org/article/738da1b18bb240f89e1c42390a1526a92021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1983276https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Gastric cancer (GC) is a common cancer with high incidence. Understanding the epidemiology and physiopathology of GC is crucial for formulating novel therapeutic strategies. Recent studies have implicated long non-coding RNA LINC00240, miR-338-5p and methyltransferase-like 3 (METTL3) in the progression of GC. In this study, we investigated the functional role of LINC00240/miR-338-5p/METTL3 axis in regulating the aggressiveness of GC cells. We first demonstrated that LINC00240 was upregulated in GC tissues and GC cell lines. High expression of LINC00240 was associated with advanced TNM stage, a higher extent of distant metastasis and lymph nodes metastasis, and the poor overall and disease-free survival of the patients. In GC cell lines, the knockdown of LINC00240 inhibited GC cell proliferation and migration, but induced cell apoptosis. We further identified and validated the functional interaction between LINC00240 and miR-338-5p. miR-338-5p seemed to function as a downstream target negatively regulated by LINC00240, and miR-338-5p could target METTL3 at 3ʹ UTR to downregulate its expression. In GC tissues, the expression of miR-338-5p was negatively correlated with LINC00240, and the expression of miR-338-5p was negatively correlated with METTL3. Importantly, miR-338-5p inhibitor or METTL3 overexpression could rescue the inhibitory effect of LINC00240 knockdown on cell proliferation and migration, and inhibit the apoptosis induction in GC cells. Taken together, our data imply that the upregulation of LINC00240 in GC cells promotes the malignant phenotype by modulating miR-338-5p/METTL3 axis, which could serve as potential therapeutic targets for GC treatment.Guoping WangZhongchen ZhangChenmei XiaTaylor & Francis Grouparticlelinc00240mir-338-5pmettl3gastric cancercell functionBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 9678-9691 (2021) |
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linc00240 mir-338-5p mettl3 gastric cancer cell function Biotechnology TP248.13-248.65 |
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linc00240 mir-338-5p mettl3 gastric cancer cell function Biotechnology TP248.13-248.65 Guoping Wang Zhongchen Zhang Chenmei Xia Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
description |
Gastric cancer (GC) is a common cancer with high incidence. Understanding the epidemiology and physiopathology of GC is crucial for formulating novel therapeutic strategies. Recent studies have implicated long non-coding RNA LINC00240, miR-338-5p and methyltransferase-like 3 (METTL3) in the progression of GC. In this study, we investigated the functional role of LINC00240/miR-338-5p/METTL3 axis in regulating the aggressiveness of GC cells. We first demonstrated that LINC00240 was upregulated in GC tissues and GC cell lines. High expression of LINC00240 was associated with advanced TNM stage, a higher extent of distant metastasis and lymph nodes metastasis, and the poor overall and disease-free survival of the patients. In GC cell lines, the knockdown of LINC00240 inhibited GC cell proliferation and migration, but induced cell apoptosis. We further identified and validated the functional interaction between LINC00240 and miR-338-5p. miR-338-5p seemed to function as a downstream target negatively regulated by LINC00240, and miR-338-5p could target METTL3 at 3ʹ UTR to downregulate its expression. In GC tissues, the expression of miR-338-5p was negatively correlated with LINC00240, and the expression of miR-338-5p was negatively correlated with METTL3. Importantly, miR-338-5p inhibitor or METTL3 overexpression could rescue the inhibitory effect of LINC00240 knockdown on cell proliferation and migration, and inhibit the apoptosis induction in GC cells. Taken together, our data imply that the upregulation of LINC00240 in GC cells promotes the malignant phenotype by modulating miR-338-5p/METTL3 axis, which could serve as potential therapeutic targets for GC treatment. |
format |
article |
author |
Guoping Wang Zhongchen Zhang Chenmei Xia |
author_facet |
Guoping Wang Zhongchen Zhang Chenmei Xia |
author_sort |
Guoping Wang |
title |
Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
title_short |
Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
title_full |
Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
title_fullStr |
Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
title_full_unstemmed |
Long non-coding RNA LINC00240 promotes gastric cancer progression via modulating miR-338-5p/METTL3 axis |
title_sort |
long non-coding rna linc00240 promotes gastric cancer progression via modulating mir-338-5p/mettl3 axis |
publisher |
Taylor & Francis Group |
publishDate |
2021 |
url |
https://doaj.org/article/738da1b18bb240f89e1c42390a1526a9 |
work_keys_str_mv |
AT guopingwang longnoncodingrnalinc00240promotesgastriccancerprogressionviamodulatingmir3385pmettl3axis AT zhongchenzhang longnoncodingrnalinc00240promotesgastriccancerprogressionviamodulatingmir3385pmettl3axis AT chenmeixia longnoncodingrnalinc00240promotesgastriccancerprogressionviamodulatingmir3385pmettl3axis |
_version_ |
1718404999774470144 |