scholarly journals Downregulated miR-1271-5p inhibits proliferation and invasion of trophoblast cells by activates Grhl2/CHL1 axis in preeclampsia

2021 ◽  
Author(s):  
Xue-Yan Shen ◽  
Li-Li Cheng ◽  
Jing Huang ◽  
Hong-Fang Kong ◽  
Ya-Jing Chang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Trophoblast Cells ◽  
Real Time Quantitative Pcr ◽  
Mediated Effects ◽  
Direct Target Gene ◽  
And Migration ◽  
Cell Adhesion Molecule L1 ◽  
And Function ◽  
Proliferation And Invasion ◽  
Proliferation And Migration

Abstract Objective: Abnormal cell growth and invasion are known to be involved in the pathogenesis of preeclampsia (PE). Previous studies have shown that miR-1271-5p promotes cell proliferation and migration. However, the expression and function of miR-1271-5p in PE still remains unclear.Materials and Methods: The expression of miR-1271-5p was detected from blood serum from pregnant and placental tissues. Silence or overexpression of miR-1271-5p in HTR8/SVneo cells. Real-time quantitative PCR was used to detect miR-1271-5p expression. Cell proliferation and invasion were determined using separately MTT assay Wound-scratch healing assay.Results: In this study, we identified a downregulation in miR-1271-5p in blood samples and placentas of PE patients compared to healthy pregnant controls. In addition, overexpression of miR-1271-5p promoted trophoblast cell proliferation and invasion, while depletion of miR-1271-5p reduced these effects. Importantly, we revealed that grainyhead-like protein 2 homolog (Grhl2), which could inhibit proliferation and migration of trophoblast cells, was a direct target gene of miR-1271-5p in primary trophoblast cells and HTR-8/SVneo cells. Furthermore, Our results showed that Grhl2 bound to the cell adhesion molecule L1-like protein (CHL1) promoter and regulated it transcription in trophoblast cells.Conclusion: Grhl2-mediated effects of miR-1271-5p on cell invasion and proliferation of trophoblast cells by promoting CHL1 transcription. The miR-1271-5p/Grhl2/CHL1 axis potentially provides a new therapeutic target for PE.

scholarly journals Long non-coding RNA HOTTIP promotes prostate cancer cells proliferation and migration by sponging miR-216a-5p

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Bin Yang ◽  
Ge Gao ◽  
Zhixin Wang ◽  
Daju Sun ◽  
Xin Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter Assay ◽  
Online Programs ◽  
Real Time Quantitative Pcr ◽  
And Migration ◽  
And Function

Long non-coding RNAs (lncRNAs) are a class of ncRNAs with >200 nts in length that regulate gene expression. The HOXA transcript at the distal tip (HOTTIP) lncRNA plays an important role in carcinogenesis, however, the underlying role of HOTTIP in prostate cancer (PCa) remains unknown. The aim of the present study was to evaluate the expression and function of HOTTIP in PCa. In the present study, we analyzed HOTTIP expression levels of 86 PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR (qPCR). Knockdown or overexpression of HOTTIP was performed to explore its roles in cell proliferation, migration, invasion, and cell cycle. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOTTIP and miR-216a-5p in PCa cells. Our results found that HOTTIP was up-regulated in human primary PCa tissues with lymph node metastasis. Knockdown of HOTTIP inhibited PCa cell proliferation, migration, and invasion. Overexpression of HOTTIP promoted cell proliferation, migration, and invasion of PCa cells. Bioinformatics online programs predicted that HOTTIP sponge miR-216a-5p at 3′-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOTTIP could negatively regulate the expression of miR-216a-5p in PCa cells. Above all, the knockdown of HOTTIP could represent a rational therapeutic strategy for PCa.

NOL6 promotes the proliferation and migration of endometrial cancer cells by regulating TWIST1 expression

Epigenomics ◽  
2021 ◽  
Author(s):  
Junhui Liang ◽  
Wenjing Sun ◽  
Hui Song ◽  
Chong Wang ◽  
Qianqian Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Cancer Cells ◽  
Ribosome Biogenesis ◽  
Tumor Formation ◽  
Tumor Xenograft ◽  
Twist1 Expression ◽  
And Migration ◽  
And Function ◽  
Proliferation And Migration

Aim: To investigate the role and function of NOL6, a protein related to ribosome biogenesis, in endometrial cancer. Methods: Methyl thiazolyl tetrazolium assay, colony formation assay, flow cytometry apoptosis assay, transwell and wound healing assays were carried out for evaluating cell proliferation, migration and apoptosis. Immunohistochemistry, western blot and tumor xenograft assays were carried out for detecting the level of protein expression and tumor formation. Results: We demonstrated that NOL6 is overexpressed in endometrial cancer and promotes cell proliferation and migration while reducing apoptosis. NOL6 regulates the expression of TWIST1, which can restore the changes in cells caused by NOL6 knockdown. Conclusions: NOL6 can promote the proliferation and migration of endometrial cancer cells by regulating TWIST1 expression.

ARFGAP3 an androgen target gene promotes prostate cancer cell proliferation and migration.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Biology ◽  
Adaptor Protein ◽  
Cancer Cell Proliferation ◽  
Lncap Cells ◽  
Gtpase Activating Protein ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

ADP ribosylation factor GTPase-activating protein 3 (ARFGAP3) is a GTPase-activating protein that associates with the Golgiapparatus and regulates the vesicular trafficking pathway. In the present study, we examined the contribution of ARFGAP3 toprostate cancer cell biology. We showed that ARFGAP3 expression was induced by 100 nM of dihydrotestosterone (DHT) atboth the mRNA and protein levels in androgen-sensitive LNCaP cells. We generated stable transfectants of LNCaP cells withFLAG-tagged ARFGAP3 or a control empty vector and showed that ARFGAP3 overexpression promoted cell proliferation andmigration compared with control cells. We found that ARFGAP3 interacted with paxillin, a focal adhesion adaptor protein thatis important for cell mobility and migration. Small interfering RNA (siRNA)-mediated knockdown of ARFGAP3 showed thatARFGAP3 siRNA markedly reduced LNCaP cell growth. Androgen receptor (AR)-dependent transactivation activity on prostatespecificantigen (PSA) enhancer was synergistically promoted by exogenous ARFGAP3 and paxillin expression, as shown byluciferase assay in LNCaP cells. Thus, our results suggest that ARFGAP3 is a novel androgen-regulated gene that can promoteprostate cancer cell proliferation and migration in collaboration with paxillin.

SOX4 Serves an Oncogenic Role in the Tumourigenesis of Human Breast Adenocarcinoma by Promoting Cell Proliferation, Migration and Inhibiting Apoptosis

2020 ◽  
Vol 15 (1) ◽  
pp. 49-58
Author(s):  
Junhe Zhang ◽  
Shujie Chai ◽  
Xinyu Ruan
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Breast Adenocarcinoma ◽  
Migration Ability ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

Background: Breast cancer is among the most common malignant cancers worldwide, and breast adenocarcinoma in glandular tissue cells has excessive metastasis and invasion capability. However, little is known on the molecular process by which this disease develops and progresses. Objective: In this study, we explored the effects of sex-determining region Y-box 4 (SOX4) protein on proliferation, migration, apoptosis and tumourigenesis of breast adenocarcinoma and its possible mechanisms. Methods: The SOX4 overexpression or knockdown Michigan Cancer Foundation-7 (MCF-7) cell lines were established. Among the SOX4 overexpression or MCF-7 knockdown cell lines, proliferation, migration ability and apoptosis rate were detected. The expression levels of apoptosis-related proteins (Bax and Cleaved caspase-3) were analysed using Western blot. The effect of SOX4 on tumourigenesis was analysed using the clone formation assay in vitro and tumour xenograft experiment in nude mice. Results: Compared with the overexpression of control cells, proliferation and migration ability of SOX4 overexpression cells significantly increased, the apoptosis rate significantly decreased in addition to the expression levels of Bax and Cleaved caspase-3 (P < 0.05). Compared with the knockdown of control cells, proliferation and migration ability of SOX4 knockdown cells significantly decreased, and the apoptosis rate and expression levels of Bax and Cleaved caspase-3 significantly increased (P < 0.05). Clone formation and tumour growth abilities of SOX4 overexpression cells were significantly higher than those of the control cells (P < 0.05), whereas SOX4 knockdown cells had the opposite effect. Conclusion: SOX4 plays an oncogenic role in breast adenocarcinoma tumourigenesis by promoting cell proliferation, migration and inhibiting apoptosis. It can be used as a potential molecular target for breast cancer gene therapy.

scholarly journals LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ye Qian ◽  
Yan Zhang ◽  
Haoming Ji ◽  
Yucheng Shen ◽  
Liangfeng Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
High Morbidity ◽  
Lipid Transfer ◽  
Protein Coding ◽  
Cell Proliferation And Migration ◽  
Reduce Cell Proliferation ◽  
And Migration ◽  
Insight Into ◽  
Proliferation And Migration

Abstract Background Lung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD. Methods The expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student’s t test or one-way analysis of variance. Results LINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells. Conclusion LINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.

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