scholarly journals The CircRNA-ACAP2/Hsa-miR-21-5p/ Tiam1 Regulatory Feedback Circuit Affects the Proliferation, Migration, and Invasion of Colon Cancer SW480 Cells

2018 ◽  
Vol 49 (4) ◽  
pp. 1539-1550 ◽  
Author(s):  
Jin-Hua He ◽  
Yu-Guang Li ◽  
Ze-Ping Han ◽  
Jia-Bin Zhou ◽  
Wei-Ming Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Target Gene ◽  
Inhibitory Effect ◽  
Sw480 Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Feedback Circuit ◽  
Sw480 Cells

Background/Aims: Circular RNAs (circRNAs), a type of RNA that is widely expressed in human cells, have essential roles in the development and progression of cancer. CircRNAs contain microRNA (miRNA) binding sites and can function as miRNA sponges to regulate gene expression by removing the inhibitory effect of an miRNA on its target gene. Methods: We used the bioinformatics software TargetScan and miRanda to predict circRNA-miRNA and miRNAi-Mrna interactions. Rate of inhibiting of proliferation was measured using a WST-8 cell proliferation assay. Clone formation ability was assessed with a clone formation inhibition test. Cell invasion and migration capacity was evaluated by performing a Transwell assay. Relative gene expression was assessed using quantitative real-time polymerase chain reaction and relative protein expression levels were determined with western blotting. circRNA and miRNA interaction was confirmed by dual-luciferase reporter and RNA-pull down assays. Results: In the present study, the miRNA hsa-miR-21-5p was a target of circRNA-ACAP2, and T lymphoma invasion and metastasis protein 1 (Tiam1) was identified as a target gene of hsa-miR-21-5p. CircRNA-ACAP2 and Tiam1 were shown to be highly expressed in colon cancer tissue and colon cancer SW480 cells, but miR-21-5p was expressed at a low level. SW480 cell proliferation was suppressed when the expression of circRNA-ACAP2 and Tiam1 was decreased and the expression of miR-21-5p was increased in vivo and in vitro. SW480 cell migration and invasion were also inhibited under the same circumstance. The circRNA-ACAP2 interaction regulated the expression of miR-21-5p, and miR-21-5p regulated the expression of Tiam1. Down-regulation of circRNA-ACAP2 promoted miR-21-5p expression, which further suppressed the transcription and translation of Tiam1. Conclusion: The present study shows that the circRNA-ACAP2/hsa-miR-21-5p/Tiam1 regulatory feedback circuit could affect the proliferation, migration, and invasion of colon cancer SW480 cells. This was probably due to the fact that circRNA-ACAP2 could act as a miRNA sponge to regulate Tiam1 expression by removing the inhibitory effect of miR-21-5p on Tiam1 expression. The results from this study have revealed new insights into the pathogenicity of colon cancer and may provide novel therapeutic targets for the treatment of colon cancer.

scholarly journals Suppression of ANT2 by miR-137 Inhibits Prostate Tumorigenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Heyuan Zhang ◽  
Nanhui Chen ◽  
Zhihai Deng ◽  
Yang Mai ◽  
Limin Deng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Target Gene ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Tumorigenesis ◽  
Direct Target Gene ◽  
Reporter Assays ◽  
Serious Disease ◽  
Cancer Tissues

Prostate cancer (PCa) is a serious disease that affects men’s health. To date, no effective and long-lasting treatment option for this condition is available in clinical practice. ANT2 is highly expressed in a variety of hormone-related cancers, but its relationship and regulatory mechanism with PCa are unclear. In this study, we found that ANT2 expression was significantly upregulated in PCa tissues relative to control samples. Genetic knockdown of ANT2 effectively inhibited, while overexpression promoted, proliferation, migration, and invasion of PCa cells. In addition, miR-137 expression was reduced in prostate cancer tissues relative to control tissues. We identified a regulatory site for miR-137 in the 3′-UTR of ANT2 mRNA; luciferase reporter assays indicated that ANT2 is a direct target gene for miR-137. Transfecting cells with miR-137 mimics and/or an ANT2-encoding plasmid revealed that ANT2 promotes proliferation, migration, and invasion of PCa, whereas co-expression of miR-137 mimics inhibited these behaviors. These observations suggest that miR-137 mimics inhibit development of PCa by antagonizing expression of ANT2. Furthermore, tumorigenic assays in nude mice showed that miR-137 inhibitors abolished the inhibitory effect of ANT2 knockdown on PCa tumor growth. Collectively, our findings suggest that ANT2, a target gene of miR-137, is intimately involved in development of PCa, providing new evidence for the mechanism underlying pathogenesis of PCa as well as new options for targeted therapy.

MiR-125b Inhibits Cell Proliferation and Induces Apoptosis in Human Colon Cancer SW480 Cells via Targeting STAT3

2021 ◽  
Vol 16 ◽  
Author(s):  
Junhe Zhang ◽  
Wenwen Yang ◽  
Yunxi Xiao ◽  
Linlin Shan
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Colon Cancer Cells ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Gene Assay ◽  
Proliferation And Apoptosis ◽  
Sw480 Cells

Background: Colon cancer is one of the most common types of cancer worldwide. Multiple studies have unveiled the key role of microRNAs (miRNAs) in the development of various types of cancer. However, the mechanism of action of miR-125b in the development and progression of colon cancer remains unknown. Objective: In this study, we explored the association of miR-125b and signal transducer and activator of transcription 3 (STAT3) and its role in the proliferation and apoptosis of SW480 colon cancer cells. Methods: The miR-125b expression in NCM460, SW480, HT29, and HCT8 cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). SW480 cells were transfected with lentiviruses of GFP–miR–125b and GFP–NC to establish a stable miR-125b overexpression colon cancer cell model and a control model. The targeting relationship between miR-125b and STAT3 was analyzed using bioinformatics and verified by the dual-luciferase reporter gene assay. Cell proliferation and apoptosis were assessed using the Cell Counting Kit-8 assay and TUNEL staining. The expression levels of STAT3, Bcl-2, and Bax were analyzed using Western blot analysis. Results: It was found that the relative mRNA expression of miR-125b was decreased in SW480, HT29, and HCT8 cells compared with that in NCM460 cells (P<0.05). The luciferase reporter gene assay confirmed that miR-125b downregulated the STAT3 gene expression (P<0.05). Overexpression of miR-125b inhibited proliferation and promoted apoptosis in SW480 colon cancer cells and was accompanied by upregulated Bax expression and downregulated Bcl-2 expression (P<0.05). Re-expression of STAT3 promoted cell proliferation and inhibited cell apoptosis, whereas Bcl-2 expression increased, and Bax expression decreased (P<0.05). Conclusion: The miR-125b regulates the expression of Bax and Bcl-2 by downregulating the expression of STAT3, thereby inhibiting proliferation and inducing apoptosis of SW480 colon cancer cells.

MiR-302a-3p, Sponged by HOXA-AS2, Suppresses Cell Proliferation and Invasion in Lung Cancer Cells

2019 ◽  
Vol 9 (12) ◽  
pp. 1644-1652
Author(s):  
Xueqin Pan ◽  
Dongchun Ma
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cell Apoptosis ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion

Lung cancer is one of the most common malignant cancers with a poor survival rate and high mortality worldwide. MiRNAs have been evaluated as crucial regulators of human gene expression, and exerted vital role involved in cancer progression. MiR-302a-3p was aberrant expressed in cancers that include pancreatic cancer and hepatocellular cancer, but its biological role in lung cancer remains elusive. This study aimed to discover the role and potential mechanism of miR-302a-3p in lung cancer. The lung cancer cell line with the highest expression of miR-302a-3p was selected, which was then subjected to transfection of miR-302a-3p mimic. Quantitative RT-PCR was performed to detect gene expression. Western blot assay was performed to determine corresponding genes that related to cell proliferation, apoptosis and invasion. Cell Counting Kit (CCK)-8 assay, flow cytometry analysis, wound healing and Transwell assay were performed to detect cell proliferation, apoptosis, migration and invasion, respectively. Luciferase reporter assay was carried out to identify the targeting relationship of miR-302-3p and HOXA-AS2. MiR-302a-3p was downregulated in lung cancer cells, and overexpression of miR-302a-3p significantly suppressed cell proliferation, migration, invasion and promoted cell apoptosis. HOXA-AS2 was a direct target of miR-302a-3p and was regulated by miR-302a-3p. HOXA-AS2 was upregulated in lung cancer cells. Upregulated HOXA-AS2 could reverse the effect that overexpression of miR-302a-3p caused on cell proliferation, apoptosis, migration and invasion. Overall, miR-302a-3p exhibited anti-oncogenic activity by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis in lung cancer by targeting HOXA-AS2, disclosing the role and regulatory mechanism of miR-302a-3p, which provided a promising therapeutic target for the clinical application of lung cancer treatment.

scholarly journals LncRNA HCG18 upregulates TRAF4/TRAF5 to facilitate proliferation, migration and EMT of epithelial ovarian cancer by targeting miR-29a/b

2022 ◽  
Vol 28 (1) ◽  
Author(s):  
Fan Zhang ◽  
Bai-Hua Luo ◽  
Qi-Hui Wu ◽  
Qing-Ling Li ◽  
Ke-Da Yang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Epithelial Ovarian Cancer ◽  
Nude Mice ◽  
Noncoding Rna ◽  
Tumour Size ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Although long noncoding RNA HLA complex group 18 (lncRNA HCG18) has been suggested to regulate cell growth in several tumours, the function of HCG18 in epithelial ovarian cancer (EOC) and its mechanism are still unclear. Methods shRNAs were applied to reduce HCG18 and related genes. For overexpression of miRNA, a miRNA mimic was transfected into cells. Quantitative real-time PCR (qRT–PCR) was used to detect levels of HCG18, miR-29a/b, and mRNAs. MTT, colony formation, wound healing and Transwell assays were used to evaluate cell proliferation, migration and invasion, respectively. A luciferase reporter assay was utilized to evaluate NF-κB activity and the binding of miRNAs with HCG18 or TRAF4/5. BALB nude mice injected with cells stably expressing shHCG18 or shNC were used for in vivo modelling. Subcutaneous tumour growth was monitored in nude mice, and immunohistochemistry (IHC) was used to determine expression of the proliferation marker Ki67. Results Abnormal expression of HCG18 and miR-29a/b was observed in EOC tissues. Knockdown of HCG18 using shRNA inhibited proliferation, migration, EMT and the proinflammatory pathway in EOC cells. miR-29a/b mimics and TRAF4/5 knockdown exhibited effects similar to HCG18 knockdown. Further experiments suggested that HCG18 directly targets miR-29a/b and upregulates TRAF4/5 expression, which are inhibited by targeting miR-29a/b. Moreover, overexpression of TRAF4/5 antagonized the inhibitory effect of HCG18 knockdown, suggesting that they are involved in HCG18-mediated oncogenic effects. Silencing HCG18 reduced tumour size and levels of Ki67 and TRAF4/5 while increasing miR-29a/b levels in vivo. Conclusions Taken together, our data revealed an oncogenic signalling pathway mediated by HCG18 in ovarian cell lines, which functions as a ceRNA of miR-29a/b and thus derepresses expression levels of TRAF4/5, facilitating NF-κB pathway-mediated promotion of EOC cell proliferation and migration.

LncRNA PCGsEM1 contributes to the Proliferation, Migration and Invasion of Non-small Cell Lung Cancer Cells via acting as a Sponge for miR-152-3p Short title: The PCGEM1/miR-152-3p axis in NSCLC

2021 ◽  
Vol 27 ◽  
Author(s):  
Jianhui Huang ◽  
Jian Lou ◽  
Xueni Liu ◽  
Yanru Xie
Keyword(s):  
Cell Proliferation ◽  
Target Gene ◽  
Biological Function ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rt Pcr ◽  
Aberrant Expression ◽  
Non Coding Rnas ◽  
Nsclc Patients ◽  
Expression Marker

Background: Long non-coding RNAs (lncRNAs) have been reported to play important roles in cellular biological function. Aberrant expression of lncRNAs has been found to be related to the progression of various diseases. LncRNA prostate cancer gene expression marker 1 (PCGEM1) has been demonstrated to be involved in the initiation and progression of human cancers. However, to date, the clinical and functional significance of PCGEM1 expression in NSCLC progression remains unknown. Methods: The expression of LncRNA PCGEM1 and miR-152-3p in NSCLC tissues and cells was analyzed using quantitative real-time RT-PCR. Experiments using NSCLC cells were conducted to explore the influence of PCGEM1 on tumor cell proliferation, migration and invasion. Results: Increased expression of PCGEM1 was observed in NSCLC tissues and cells compared with the corresponding controls (all P < 0.001). PCGEM1 expression was associated with NSCLC patients’ lymph node metastasis and TNM stage (all P < 0.05), and the knockdown of PCGEM1 in NSCLC cells led to inhibited cell proliferation, migration and invasion. The further luciferase reporter assay and expression results showed that miR-152-3p might be a target gene of PCGEM1 and mediate the effects of PCGEM1 on cell proliferation, migration and invasion in NSCLC. Conclusion: Thus, the findings from the present study indicate that the NSCLC patients have significantly increased PCGEM1 and decreased miR-152-3p expression and that the knockdown of PCGEM1 may inhibit NSCLC cell proliferation, migration and invasion by sponging miR-152-3p. The PCGEM1/miR-152-3p axis may provide novel therapeutic targets for NSCLC treatment.

scholarly journals miR-215 Inhibits Colorectal Cancer Cell Migration and Invasion via Targeting Stearoyl-CoA Desaturase

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Xinhua Xu ◽  
Yan Ding ◽  
Jun Yao ◽  
Zhiping Wei ◽  
Haipeng Jin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Target Gene ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter Assay ◽  
Cell Migration And Invasion ◽  
Stearoyl Coa Desaturase

Background. This study was aimed at exploring the effects of miR-215 and its target gene stearoyl-CoA desaturase (SCD) on colorectal cancer (CRC) cell migration and invasion. Methods. Here, we analyzed the relationship between miR-215 and SCD, as well as the regulation of miR-215 on CRC cells. We constructed wild-type and mutant plasmids of SCD to identify whether SCD was a target gene of miR-215 by using a luciferase reporter assay. The expression of miR-215 and SCD was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot, respectively. MTT, wound healing, and Transwell assays were applied to determine the effect of miR-215 on CRC cell proliferation, migration, and invasion. Results. It was found that miR-215 expression was significantly decreased in CRC tissue while SCD was highly expressed compared with those in adjacent normal tissue. The luciferase reporter assay indicated that SCD was a direct target gene of miR-215. Functional analysis revealed that miR-215 overexpression significantly inhibited CRC cell proliferation, migration, and invasion in vitro. In addition, the result of rescue experiments showed that overexpression of SCD could promote the proliferation, migration, and invasion of CRC cells, and the carcinogenic effect of SCD could be inhibited by miR-215. Conclusions. Taken together, our findings suggested that miR-215 could inhibit CRC cell migration and invasion via targeting SCD. The result could eventually contribute to the treatment for CRC.

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-182-5p Serves as an Oncogene in Lung Adenocarcinoma through Binding to STARD13

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Xuhui Wu ◽  
Wei Wang ◽  
Gongzhi Wu ◽  
CongXiong Peng ◽  
Jichun Liu
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Untranslated Region ◽  
Target Gene ◽  
Bioinformatics Analysis ◽  
Inverse Correlation ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Prevalent Subtype

Lung cancer as one of the commonest invasive malignancies is featured by high morbidity and mortality, wherein lung adenocarcinoma (LUAD) is the most prevalent subtype. Accumulating evidence exhibited that microRNAs are involved in LUAD occurrence and progression. In this study, miR-182-5p was observed to increase in both LUAD tissue and cell lines. Overexpression of miR-182-5p could prominently facilitate cell proliferation, migration, and invasion in LUAD. Through bioinformatics analysis, STARD13 was theorized as the target gene of miR-182-5p, which was lowly expressed in LUAD. Further molecular experiments manifested that miR-182-5p bound to the 3 ′ -untranslated region of STARD13, and there was an inverse correlation between STARD13 and miR-182-5p in LUAD. Rescue experiments demonstrated that silencing STARD13 conspicuously restored the inhibitory effect of decreased miR-182-5p on cell proliferation, migration, and invasion in LUAD. Together, our findings revealed novel roles of the miR-182-5p/STARD13 axis in LUAD progression.

scholarly journals Functional analyses of microRNA-326 in breast cancer development

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Ye Du ◽  
Lishengnan Shen ◽  
Wei Zhang ◽  
Rongbo Ding ◽  
Qian Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Human Breast Cancer ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Breast ◽  
Promising Therapeutic Target ◽  
G0 Phase

Abstract MicroRNA-326 (miR-326) was reported to be dysregulated and involved in the progression of multiple cancers. However, the clinical significance, biological role and underlying mechanism of miR-326 in the carcinogenesis of breast cancer are still unclear. In the present study, we showed that miR-326 was down-regulated in human breast cancer tissues and cell lines. Our results also revealed that miR-326 overexpression significantly suppressed breast cancer cell proliferation, migration and invasion, and induced cell cycle arrest at G1/G0 phase. Furthermore, Sex determining region Y-box (SOX) protein 12 (SOX12), a known oncogene, was identified as a direct target of miR-326 by luciferase reporter assay. Moreover, miR-326 expression was inversely correlated with SOX12 mRNA expression levels in human breast cancer specimens. Overexpression of SOX12 partially rescued the inhibitory effect on cell proliferation, migration and invasion in breast cancer cells caused by miR-326 overexpression. These findings suggested that miR-326 might play a suppressive role in breast cancer, at least in part, by targeting SOX12, rendering miR-326 a promising therapeutic target for breast cancer.

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