LncRNA MCM3AP-AS1 sponges miR-148a to enhance cell invasion and migration in small cell lung cancer

Abstract Background MCM3AP-AS1 is a recently characterized lncRNA playing an oncogenic role in several cancers. However, its role in lung cancer remains unknown. Here, we aimed to explore the functions of MCM3AP-AS1 in small cell lung cancer (SCLC) and the possible underlying mechanisms. Methods MCM3AP-AS1 and ROCK1 levels in SCLC patients were analyzed by qPCR. RNA pull-down and luciferase assays were performed to analyze the interaction between MCM3AP-AS1 and miR-148a. ROCK1 mRNA and protein levels were detected by qPCR and Western blot, respectively. Cell invasion and migration were analyzed by Transwell assays. Results MCM3AP-AS1 was upregulated in patients with SCLC, and a high MCM3AP-AS1 level was accompanied by a low survival rate. The binding of MCM3AP-AS1 to miR-148a predicted by bioinformatics analysis was verified by RNA pull-down and luciferase assays. However, MCM3AP-AS1 and miR-148a did not affect each other’s expression. ROCK1 was upregulated in SCLC tissues and positively correlated with MCM3AP-AS1. In SCLC cells, MCM3AP-AS1 overexpression increased ROCK1 and promoted cancer cell invasion and migration, while miR-148a overexpression showed the opposite effects and attenuated the effects of MCM3AP-AS1 overexpression on ROCK1 expression and cell behaviors. Conclusions MCM3AP-AS1 sponges miR-148a, thereby increasing SCLC cell invasion and migration via upregulating ROCK1 expression.

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LncRNA PSMG3-AS1 Downregulates miR-340 through Methylation to Upregulate ROCK1 and Promote Cell Invasion and Migration in Non-small Cell Lung Cancer

10.21203/rs.3.rs-153993/v1 ◽

2021 ◽

Author(s):

Xiyong Wang ◽

Yang Yang ◽

Yu Dai ◽

Hongming Zhang ◽

Honglin Xia ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Cell Invasion ◽

Mirna Gene ◽

Small Cell ◽

Small Cell Lung ◽

Invasion And Migration ◽

And Migration

Abstract Background: LncRNA PSMG3‑AS1 plays oncogenic role in breast cancer. However, its role in non-small cell lung cancer (NSCLC) is hardly known. We then studied the role of PSMG3‑AS1 in NSCLC.Methods: RT-qPCR was performed to determine the expression of PSMG3‑AS1 in NSCLC and non-tumor tissues from 60 NSCLC patients. A survival analysis was carried out to visit patients for 5 years to study the role PSMG3‑AS1 in prediction the survival of NSCLC. NSCLC cells were overexpressed with miR-340 or PSMG3‑AS1 to analyze the crosstalk between PSMG3‑AS1 and miR-340. MSP was performed to analyze the methylation of miR-340 miRNA gene. The invasion and migration abilities of cells were determind by Transwell assays.Results: PSMG3‑AS1 was highly expressed in NSCLC and was closely correlated poor survival. PSMG3‑AS1 and miR340 were inversely correlated. In NSCLC cells, PSMG3‑AS1 decreased the expression of miR-340 and increased methylation of miR-340 gene. However, miR-340 overexpression did not significantly affect the expression of PSMG3‑AS1. In addition, PSMG3‑AS1 overexpression resulted in upregulated expression of ROCK1. PSMG3‑AS1 and ROCK1 overexpression increased cell invasion and migration rates. MiR-340 overexpression suppressed cell behaviors and inhibited the role of PSMG3‑AS1.Conclusions: PSMG3‑AS1 may downregulate miR-340 through methylation to upregulate ROCK1 and promote cell invasion and migration in NSCLC.

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LncRNA LINC01116 sponges miR-93-5p to promote cell invasion and migration in small cell lung cancer

BMC Pulmonary Medicine ◽

10.1186/s12890-020-01369-3 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Wenzhou Liu ◽

Feihai Liang ◽

Guangyu Yang ◽

Lei Xian

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Expression Analysis ◽

Cell Lung Cancer ◽

Cell Invasion ◽

Small Cell ◽

Small Cell Lung ◽

Cell Behaviors ◽

Invasion And Migration ◽

And Migration

Abstract Background LINC01116 is a recently identified oncogenic lncRNA in glioma. Differential expression analysis using the public gene expression analysis tool GEPIA revealed the upregulation of LINC01116 in lung cancer. We studied the functions of LINC01116 in small cell lung cancer (SCLC). Methods The expression of LINC01116 in several types of cancer tissue and the paired non-tumor tissues was evaluated by GEPIA. The effects of the overexpression of LINC01116 and miR-93-5p on the expression of STAT3 were evaluated. The effects of the overexpression of LINC01116, miR-93-5p and STAT3 on SHP-77 cell behaviors were evaluated by Transwell assays. Results LINC01116 was highly expressed in SCLC and predicted poor survival. In SCLC tissues, the expression of LINC01116 was positively correlated with STAT3. Bioinformatics analysis revealed that miR-93-5p may target LINC01116. Overexpression of LINC01116 increased STAT3 but did not affect the expression of miR-93-5p. Transwell assay showed that LINC01116 and STAT3 increased cell invasion and migration rates. MiR-93-5p played an suppressed cell behaviors and suppressed the role of LINC01116. Conclusion Therefore, LINC01116 might upregulate STA3 by sponging miR-93-5p, thereby promoting cell invasion and migration in SCLC.

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LncRNA LUADT1 sponges miR-15a-3p to upregulate Twist1 in small cell lung cancer

BMC Pulmonary Medicine ◽

10.1186/s12890-019-0991-7 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 2

Author(s):

Dingxue Wang ◽

Wenyu Wu ◽

Wenqi Huang ◽

Jinghui Wang ◽

Li Luo ◽

...

Keyword(s):

Lung Cancer ◽

Lung Adenocarcinoma ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Cell Invasion ◽

Small Cell ◽

Small Cell Lung ◽

Invasion And Migration ◽

And Migration ◽

Rna Interaction

Abstract Lung adenocarcinoma associated transcript 1 (LUADT1) has been reported as an oncogenic long non-coding RNA (lncRNA) in lung adenocarcinoma, while its roles in small cell lung cancer (SCLC) are unknown. Our RNA interaction bioinformatics prediction showed that LUADT1 could form strong base pairing with miR-15a-3p, which is a tumor-suppressive miRNA that can target Twist1. We found that LUADT1 and Twist1 were upregulated in SCLC, while miR-15a-3p was downregulated in SCLC. However, LUADT1 was posively correlated with Twist1 but was not significnatly correlated with miR-15a-3p. Overexpression experiments showed that and LUADT1 and miR-15a-3p did not significantly affect the expression of each other. Moreover, LUADT1 overexpression mediated the upregualtion of Twist1, and miR-15a-3p overexpression played an oppsoite role. Transwell assays showed that LUADT1 and Twist1 overexpression mediated the increased rate of cell invasion and migration, while miR-15a-3p overexpression mediated the decreased rate of cell invasion and migration. In addition, miR-15a-3p overexpression played an oppsoite role and attenuated the effects of LUADT1 overexpression. Therefore, LUADT1 may sponge miR-15a-3p to upregulate Twist1 in SCLC, thereby promoting cancer cell invasion and migration. Trial registration 2017GZH-1-201,746,382, registered at Jan 02,2017.

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LncRNA MCM3AP-AS1 sponges miR-148a to cell invasion and migration in small cell lung cancer

10.21203/rs.3.rs-41537/v1 ◽

2020 ◽

Author(s):

Hua Luo ◽

Yu Kun Zhang ◽

Guang Mei Qin ◽

Bing Jiang ◽

Li li Miao

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Cell Invasion ◽

Small Cell ◽

Gene Interactions ◽

Small Cell Lung ◽

Invasion And Migration ◽

Migration Rates ◽

And Migration

Abstract Background: MCM3AP-AS1 is a recently characterized lncRNA in hepatocellular carcinoma (HCC) and (GBM). We found that miR-148a may be able to bind MCM3AP-AS1. We explored the functions of lncRNA MCM3AP-AS1 in small cell lung cancer (SCLC). Methods: Gene expression in SCLC patients was analyzed by qPCR. Transient transfections were performed to analyze gene interactions. Cell invasion and migration were analyzed by Transwell assays.Results: We found that MCM3AP-AS1 was upregulated in SCLC and high expression levels were accompanied by low survival rate. Bioinfromatics analysis showed that MCM3AP-AS1 may bind miR-148a, which can target ROCK1. In SCLC tissues, MCM3AP-AS1 was positively correlated with ROCK1. In SCLC cells, MCM3AP-AS1 overexpression mediated the upregulated ROCK1 expression and increased cell invasion and migration rates. However, MCM3AP-AS1 and miR-148a could not regulate each other. However, miR-148a overexpressed led to downregulated ROCK1 expression, decreased cell invasion and migration rates, and reduced effects of MCM3AP-AS1 overexpression. Conclusions: Therefore, MCM3AP-AS1 may sponge miR-148a to cell invasion and migration in SCLC through the upregulation of ROCK1.

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