scholarly journals miR-139-5p Inhibits Lung Adenocarcinoma Cell Proliferation, Migration, and Invasion by Targeting MAD2L1

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Jianfeng Li ◽  
Xi He ◽  
Xiaotang Wu ◽  
Xiaohui Liu ◽  
Yixiong Huang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Differential Analysis ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
Mirna Expression Data

Background. miR-139-5p is lowly expressed in various human cancers and exerts its antitumor effect through different molecular mechanisms, yet the molecular mechanism of miR-139-5p in lung adenocarcinoma (LUAD) remains to be further elucidated. The study is aimed at investigating the role and the regulatory mechanism of miR-139-5p in LUAD progression. Methods. Differential analysis was performed on miRNA expression data in the TCGA-LUAD dataset. qRT-PCR was employed to detect the transcription levels of miR-139-5p and MAD2L1 in LUAD cells, while western blot was carried out for the detection of MAD2L1 protein expression. CCK-8 and Transwell assays were implemented to assess LUAD cell proliferation, migration, and invasion. A dual-luciferase reporter gene assay was conducted to verify the direct targeting relationship between miR-139-5p and MAD2L1. Results. miR-139-5p was significantly downregulated in LUAD cells in comparison with that in human normal bronchial epithelial cells. Overexpressing miR-139-5p inhibited LUAD cell proliferation, migration, and invasion, while opposite results could be observed when miR-139-5p was inhibited. MAD2L1 was identified as a direct target of miR-139-5p in LUAD. Besides, the inhibitory effect of miR-139-5p overexpression on LUAD cell proliferation, migration, and invasion was attenuated by overexpressing MAD2L1. Conclusion. Our study suggests that miR-139-5p is lowly expressed in LUAD cells and inhibits LUAD cell proliferation, migration, and invasion by targeted suppressing MAD2L1 expression. It is of potential significance for the prognosis and treatment of LUAD.

scholarly journals miR-301b-3p promotes lung adenocarcinoma cell proliferation, migration and invasion by targeting DLC1

2020 ◽  
Author(s):  
Haitao Liu ◽  
Xingjie Ma ◽  
Niu Niu ◽  
Junjie Zhao ◽  
Chao Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Promoting Effect ◽  
Luciferase Reporter Gene Assay ◽  
Gene Assay ◽  
Underlying Mechanisms

Abstract Background miR-301b-3p has been reported to be abnormally expressed in various human cancers including lung cancer. However, the underlying role and molecular mechanisms in lung adenocarcinoma (LUAD) remain unclear. This study aimed to elucidate the underlying mechanisms of miR-301b-3p in LUAD. Methods Based on TCGA database, we found that miR-301b-3p was prominently up-regulated in LUAD tissues. A series of functional experiments including CCK-8 assay, colony formation assay and Transwell assay uncovered that the up-regulation of miR-301b-3p facilitated LUAD cell proliferation, migration and invasion abilities. Bioinformatics analysis and dual-luciferase reporter gene assay demonstrated that Deleted in Liver Cancer 1 (DLC1) was negatively regulated by miR-301b-3p, and it was extremely lowly expressed in LUAD tissues and cells. Results Rescue experiments suggested that overexpressing DLC1 restored the promoting effect of miR-301b-3p on LUAD cell proliferation, migration and invasion. Conclusions Taken together, our study elucidated that miR-301b-3p promoted LUAD cell proliferation, migration and invasion by targeted suppressing DLC1 expression. The discovery of the mechanism provides a novel therapeutic strategy for LUAD patients, which helps to improve the survival of patients.

scholarly journals PITPNA-AS1 Activated by H3K27ac Sponged miR-98-5p to Regulate Cisplatin Resistance in Gastric Cancer

2021 ◽  
Author(s):  
Yaping Liu ◽  
Xu Zhao ◽  
Yinnan Chen ◽  
Gang Guo ◽  
Jiansheng Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Platinum Resistance ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
Proliferation And Apoptosis ◽  
Gastric Cancer Cell Lines ◽  
Cancer Tissues

Abstract To evaluate the expression of PITPNA-AS1 and miR-98-5p in gastric cancer tissues as well as their association with progression of gastric cancer, and investigate the role of PITPNA-AS1 and miR-98-5p in developing platinum resistance. RNA sequencing was used to identify candidate lncRNAs and microRNAs related to local recurrence of gastric cancer. qRT-PCR was used to investigate the expression of PITPNA-AS1 and miR-98-5p. CCK-8 and caspase3/7 activity were used to evaluate the cell proliferation and apoptosis rate. Dual luciferase reporter gene assay and RNA pull down were used to evaluate the cross talk between PITPNA-AS1 and miR-98-5p. PITPNA-AS1 and miR-98-5p could regulate cell proliferation and inhibit apoptosis in gastric cancer cell lines. Cisplatin and lobaplatin could significantly suppress the expression of PITPNA-AS1, which interacted with negatively regulated miR-98-5p expression. PITPNA-AS1 overexpression impaired the effect of platinum, which was partially reversed by downregulation of miR-98-5p knock down. In gastric cancer, PITPNA-AS1 and miR-98-5p could regulat cell growth, apoptosis and platinum resistance. They have the potential to be biomarkers and curative therapeutic targets. However, further research on molecular mechanisms are needed.

scholarly journals Hsa_circ_0000520 is Involved in Breast Cancer Progression by Targeting miR-542-3p/S1PR1 Axis

2021 ◽  
Author(s):  
Jianjie Zhao ◽  
Xueqin Wang ◽  
Juan Jiang ◽  
Yao Ding ◽  
qinan wu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Multiplication ◽  
Sample Collection ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Abstract Background: CircRNAs feature prominently in breast cancer (BC) progression. This study was intended to investigate the role of hsa_circ_0000520 in BC progression.Methods: After the sample collection, quantitative real-time polymerase chain reaction (qRT-PCR) was conducted for quantifying the expressions of circ_0000520, miR-542-3p, and sphingosine-1-phosphate receptor 1 (S1PR1) mRNA. 5‐Ethynyl‐2′‐Deoxyuridine (EdU) and cell counting kit-8 (CCK-8) assays were used for measuring cell proliferation. Transwell assays were employed to detect cell migration and invasion. Western blotting was utilized for analyzing S1PR1 protein expression. Dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to delve into the targeting relationship between circ_0000520 and miR-542-3p.Results: Circ_0000520 expression was markedly elevated in BC cell lines and tissues, and knockdown of circ_0000520 could inhibit BC cell multiplication, migration, and invasion. Circ_0000520 could target miR-542-3p to negatively regulate S1PR1 expression. S1PR1 overexpression plasmid could counteract the inhibitory effects of circ_0000520 knockdown on BC cell proliferation, migration, and invasion.Conclusion: Circ_0000520, as a cancer-promoting circRNA, participates in BC progression by regulating miR-542-3p/S1PR1 axis.

scholarly journals MiR-4310 Induced by SP1 targets PTEN to Promote Glioma Progression

2020 ◽  
Author(s):  
Wu Zhiyong ◽  
Luo Jie ◽  
Huang Tengyue ◽  
Yi Renhui ◽  
Ding Shengfeng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Luciferase Reporter Gene ◽  
Mobility Shift ◽  
Glioma Progression

Abstract Background: miRNAs have been reported to be involved in multiple biological processes of gliomas. Here, we aimed to analyze miR-4310 and its correlation genes involved in the tumor progression of human glioma.Methods: miR-4310 expression levels were examined in glioma and non-tumor brain (NB) tissues. The molecular mechanisms of miR-4310 expression and its effects on cell proliferation, migration, and invasion were explored by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) , Transwell chamber, Boyden chamber, and western blot analyses, as well as in vivo tumorigenesis in nude mice. The relationships among miR-4310, SP1, and phosphatase and tensin homolog (PTEN) were explored by chromatin immunoprecipitation (ChIP), agarose gel electrophoresis, electrophoresis mobility shift (EMSA), and dual luciferase reporter gene assays. Results: miR-4310 expression was upregulated in glioma tissues compared to NB. Overexpressed miR-4310 promoted glioma cell proliferation, migration, and invasion in vitro and tumorigenesis in vivo . Inhibition of miR-4310 was sufficient to reverse these results. Mechanistic analyses revealed that miR-4310 promoted glioma progression through the PI3K/AKT pathway by targeting PTEN. Additionally, SP1 induced the expression of miR-4310 by binding to its promoter region. Conclusion: miR-4310 promotes the progression of glioma by targeting PTEN and activating the PI3K/AKT pathway meanwhile the expression of miR-4310 is induced by SP1.

scholarly journals MiR-4310 induced by SP1 targets PTEN to promote glioma progression

2020 ◽  
Author(s):  
Wu Zhiyong ◽  
Luo Jie ◽  
Huang Tengyue ◽  
Yi Renhui ◽  
Ding Shengfeng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Luciferase Reporter Gene ◽  
Mobility Shift ◽  
Glioma Progression

Abstract Background: miRNAs have been reported to be involved in multiple biological processes of gliomas. Here, we aimed to analyze miR-4310 and its correlation genes involved in the tumor progression of human glioma. Methods: miR-4310 expression levels were examined in glioma and non-tumor brain (NB) tissues. The molecular mechanisms of miR-4310 expression and its effects on cell proliferation, migration, and invasion were explored by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) , Transwell chamber, Boyden chamber, and western blot analyses, as well as in vivo tumorigenesis in nude mice. The relationships among miR-4310, SP1, and phosphatase and tensin homolog (PTEN) were explored by chromatin immunoprecipitation (ChIP), agarose gel electrophoresis, electrophoresis mobility shift (EMSA), and dual luciferase reporter gene assays. Results: miR-4310 expression was upregulated in glioma tissues compared to NB. Overexpressed miR-4310 promoted glioma cell proliferation, migration, and invasion in vitro and tumorigenesis in vivo . Inhibition of miR-4310 was sufficient to reverse these results. Mechanistic analyses revealed that miR-4310 promoted glioma progression through the PI3K/AKT pathway by targeting PTEN. Additionally, SP1 induced the expression of miR-4310 by binding to its promoter region. Conclusion: miR-4310 promotes the progression of glioma by targeting PTEN and activating the PI3K/AKT pathway meanwhile the expression of miR-4310 is induced by SP1.

scholarly journals miR-196a-2 Promotes Malignant Progression of Thyroid Carcinoma by Targeting NRXN1

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Yaohua Fan ◽  
MingJian Fei ◽  
Yan Li ◽  
Zhenzhen Gao ◽  
Yuzhang Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Promoting Effect ◽  
Promote Cell Proliferation ◽  
Study Results ◽  
Gene Assay ◽  
Molecular Therapeutic

Thyroid cancer (TC) is the most common endocrine malignant disease with a rising morbidity year by year. Accumulating studies have shown that microRNAs (miRNAs) play a regulatory role in the progression of various tumors, but the molecular regulatory mechanism of miR-196a-2 in TC is still unknown. qRT-PCR was employed to measure the expression of miR-196a-2 and NRXN1 mRNA in TC cells, while western blot was used to detect the protein expression of NRXN1. CCK-8, colony formation and flow cytometry assays were used to measure cell proliferation and apoptosis of TC cells. Dual-luciferase reporter gene assay was used to predict and verify the targeted binding relationship between miR-196a-2 and NRXN1. Our study results manifested that miR-196a-2 was dramatically overexpressed in cells of TC, while NRXN1 was lowly expressed. miR-196a-2 could promote cell proliferation and inhibit cell apoptosis of TC. Additionally, miR-196a-2 could also target and inhibit the expression of NRXN1. Silencing NRXN1 could reverse the inhibitory effect of miR-196a-2 downregulation on cell proliferation of TC, as well as the promoting effect on cell apoptosis. In a conclusion, we found that miR-196a-2 could promote cell proliferation and inhibit cell apoptosis of TC by targeting NRXN1. Therefore, miR-196a-2/NRXN1 is potential to be a molecular therapeutic target for TC.

Upregulation of circ_0000142 promotes multiple myeloma progression by adsorbing miR-610 and upregulating AKT3 expression

2020 ◽  
Author(s):  
Fang Liu ◽  
Yan-Li Wang ◽  
Jie-Mei Wei ◽  
Zhao-Dong Huang
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Expression Level ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Clinicopathological Parameters ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Abstract Circular RNAs (circRNAs) play an important regulatory role in a variety of malignancies. Nevertheless, the role of circ_0000142 in multiple myeloma (MM) and its regulatory mechanism remains largely unknown. Real-time polymerase chain reaction was employed to detect the expressions of circ_0000142 and miR-610 in MM tissues and cell lines. The expression of AKT3 and apoptosis-related proteins (Bcl-2, Bax) in MM cells was detected by western blot. The correlation between the expression level of circ_0000142 and the clinicopathological parameters of MM patients was analysed. Cell proliferation, apoptosis, migration and invasion were monitored by Cell Counting Kit 8 assay, flow cytometry analysis and Transwell assay, respectively. The dual-luciferase reporter gene assay and RNA immunoprecipitation assay were employed to verify the targeting relationship between circ_0000142 and miR-610. In this study, it was demonstrated that, circ_0000142 was highly expressed in MM patients, and its high expression level was significantly associated with increased International Staging System and Durie–Salmon stage. Overexpression of circ_0000142 enhanced MM cell proliferation, migration, invasion and suppressed cell apoptosis, while knocking down circ_0000142 had the opposite effects. Mechanistically, circ_0000142 functioned as a competitive endogenous RNA, directly targeting miR-610 and positively regulating AKT3 expression. In brief, circ_0000142 enhances the proliferation and metastasis of MM cells by modulating the miR-610/AKT3 axis.

scholarly journals Decreased miR- 31 Suppress Cell Migration and Proliferation By Targeting Syncytin-1 in Pancreatic Carcinoma

2020 ◽  
Author(s):  
Jing Yang ◽  
Judong Luo ◽  
Feng Wang ◽  
Zhiwen Cheng ◽  
Xia Han ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Prognostic Significance ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Kaplan Meier ◽  
Gene Assay ◽  
Proliferation And Invasion

Abstract Background: Pancreatic cancer(PC) is seriously harmful to human health, and the pathogenesis is not clear. The present study aimed to explore the functional role of syncytin-1 in PC.Methods: Syncytin-1 and miR-31 expression was analyzed by qRT-PCR and Western blot analysis in both human PC cell lines and tissuse. The prognostic significance of syncytin-1 was investigated using the immunohistochemistry(IHC) and Kaplan-Meier survival. The CCK-8 assay and transwell assays were used to determine the role of syncytin-1 and miR-31 in cell proliferation, migration and invasion. Luciferase reporter assays was used to identify possible miRNA targets in tumorigenesis.Results: The results showed that the syncytin-1 level was significantly decreased in PC cell lines and tissues than normal(P < 0.05), while miR-31 was markedly higher than normal(P < 0.05), and low expression of syncytin-1 have a poor prognosis than high expression(P < 0.05). Overexpression of syncytin-1 significantly reduced the PC cell proliferation and invasion ability in PANC-1 and BxPC-3 cells(P < 0.05), and miR-31showed contrary results. The Dual-Luciferase reporter gene assay demonstrated that miR-31 binded directly to 3’UTR of syncytin-1 and resulting in the inhibition of syncytin-1. The overexpression of miR-31 promoted migration and proliferation of PC cells through down-regulating the expression of syncytin-1.Conclusion: We verified that syncytin-1 can inhibit proliferation and invasion of PC cell lines by targeting miR-31.

scholarly journals LncRNA LINC00337 sponges mir-1285-3p to promote proliferation and metastasis of lung adenocarcinoma cells by upregulating YTHDF1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ru-nan Zhang ◽  
Dong-mei Wu ◽  
Li-ping Wu ◽  
Guo-wei Gao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Gear Up ◽  
Underlying Mechanisms

Abstract Background Emerging studies have shown that long noncoding RNAs (lncRNAs) predominantly function in the carcinogenesis of multiple developing human tumors. The current study aimed to investigate the underlying mechanisms of LINC00337 in lung adenocarcinoma. Methods We analyzed TCGA and GTEx datasets and chose LINC00337 as the research object. Cell proliferation, cell apoptosis, cell cycle, migration, and invasion were detected in the gain and loss experiments of LINC00337 both in vitro and in vivo. Moreover, RNA pull-down, luciferase reporter assays, western blotting analysis, and rescue experiments were performed to investigate the underlying molecular mechanisms of LINC00337 function. Results LINC00337 expression was remarkably upregulated in lung adenocarcinoma. In addition, LINC00337 knockdown was shown to repress cell migration, invasion, and proliferation, as well as the cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. With respect to the mechanism, LINC00337 knockdown boosted miR-1285-3p expression and then restrained YTHDF1 expression post-transcriptionally. Crucially, both miR-1285-3p decrement and YTHDF1 overexpression successfully reversed the influence on cell proliferation, migration, invasion, and apoptosis caused by LINC00337 shRNA. Conclusions These results suggest that LINC00337 acts as an oncogenic lncRNA, targeting miR-1285-3p and regulating YTHDF1 expression, to promote the progression of lung adenocarcinoma.

scholarly journals miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Linsen Feng ◽  
Jianhua Ma ◽  
Haiming Ji ◽  
Yichun Liu ◽  
Weixing Hu
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Biological Effects ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Normal Brain ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Gene Assay ◽  
And Migration

The present study intended to investigate the biological effects of miR-330-5p on glioblastoma (GBM) cell proliferation and invasiveness by targeting integrin α5 (ITGA5). The expressions of miR-330-5p and ITGA5 mRNA in GBM cell lines (U87, U251, and U373) and normal brain glial cell line (HEB) were detected using RT-qPCR. Protein expression of ITGA5 was examined using Western blot. The present study used MTT assay, colony formation assay, Transwell assay, wound healing assay, and flow cytometry analysis in order to determine the biological functions of GBM cells (including cell proliferation, invasion, migration, apoptosis, and cell cycle). The present study applied dual-luciferase reporter gene assay to identify the target relationship between miR-330-5p and ITGA5. miR-330-5p was low-expressed in GBM cell lines while ITGA5 was high-expressed compared with HEB. miR-330-5p could directly target ITGA5 as well as suppress its expression in GBM cells. Up-regulation of miR-330-5p and down-regulation of ITGA5 both have an inhibitory effect on cell proliferation, invasion, and migration. Meanwhile, they could also promote GBM cell apoptosis. miR-330-5p could suppress proliferation and invasion of GBM cells through targeting ITGA5.

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