scholarly journals LncRNA PVT1 promotes proliferation and invasion through enhancing Smad3 expression by sponging miR-140-5p in cervical cancer

2019 ◽  
Vol 53 (4) ◽  
pp. 443-452 ◽  
Author(s):  
Qing-Qing Chang ◽  
Chun-Yan Chen ◽  
Zhao Chen ◽  
Shuai Chang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Bioinformatics Analysis ◽  
Downstream Target ◽  
Cervical Cancer Cells ◽  
Proliferation And Metastasis ◽  
Underlying Mechanisms ◽  
Smad3 Expression ◽  
Proliferation And Invasion ◽  
Variant Translocation

Abstract Background Cervical cancer is one of the most frequent malignancies among females worldwide. Increasing evidence have indicated the participation of long noncoding RNAs (lncRNAs) in the progression and metastasis of cervical cancer. Our present study was conducted to explore the effects of lncRNA plasmacytoma variant translocation 1 (PVT1) on the progression of cervical cancer and the underlying mechanisms. Materials and methods Expressions of PVT1, miR-140-5p and Smad3 in cervical cancer cell lines were detected by qRT-PCR and western blotting. Bioinformatics analysis and luciferase assays were used to elucidate the potential correlations between PVT1, miR-140-5p and Smad3. The roles of PVT1 on the progression of cervical cancer cells were determined by transfecting sh-RNA through series function assays such as colony formation assay, wound healing assay, transwell assay. Results PVT1 and Smad3 were upregulated, and miR-140-5p was downregulated in cervical cancer cells. PVT1 could bind directly with miR-140-5p, and Smad3 was a downstream target of miR-140-5p. Inhibition of PVT1 could enhance expression of miR-140-5p, inhibit the expression of Smad3, significantly inhibited the proliferation, migration, invasion in cervical cancer cells. While transfection of miR-140-5p inhibitor could partially reverse the above changes in cervical cancer cells. Conclusions The results revealed that PVT1 could promote the proliferation and metastasis via increasing the Smad3 expression by sponging miR-140-5p, which might be a promising prognostic and therapeutic target for cervical cancer.

scholarly journals Stanniocalcin1 (STC1) Inhibits Cell Proliferation and Invasion of Cervical Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e53989 ◽  
Author(s):  
Fengjie Guo ◽  
Yalin Li ◽  
Jiajia Wang ◽  
Yandong Li ◽  
Yuehui Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Proliferation And Invasion

scholarly journals HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targetting miR-23b/MAPK1 axis

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Qin Li ◽  
Yanhong Feng ◽  
Xu Chao ◽  
Shuai Shi ◽  
Man Liang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Tissue ◽  
Tissue Samples ◽  
Downstream Target ◽  
Cervical Cancer Cells

The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) has been found to be overexpressed in many human malignancies and involved in tumor progression and metastasis. Although the downstream target through which HOTAIR modulates tumor metastasis is not well-known, evidence suggests that miR-23b might be involved in this event. In the present study, the expressions of HOTAIR and miR-23b were detected by real-time PCR in 33 paired cervical cancer tissue samples and cervical cell lines. The effects of HOTAIR on the expressions of miR-23b and mitogen-activated protein kinase 1 (MAPK1) were studied by overexpression and RNAi approaches. We found that HOTAIR expression was significantly increased in cervical cancer cells and tissues. In contrast, the expression of miR-23b was obviously decreased. We further demonstrated that HOTAIR knockdown promoted apoptosis and inhibited cell proliferation and invasion in vitro and in vivo. Moreover, our data indicated that HOTAIR may competitively bind miR-23b and modulate the expression of MAPK1 indirectly in cervical cancer cells. Taken together, our study has identified a novel pathway through which HOTAIR exerts its oncogenic role, and provided a molecular basis for potential applications of HOTAIR in the prognosis and treatment of cervical cancer.

scholarly journals Interleukin 37 Expression Inhibits STAT3 to Suppress the Proliferation and Invasion of Human Cervical Cancer Cells

2015 ◽  
Vol 6 (10) ◽  
pp. 962-969 ◽  
Author(s):  
Sen Wang ◽  
Weifang An ◽  
Yunhong Yao ◽  
Renhuai Chen ◽  
Xiaoxuan Zheng ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Proliferation And Invasion ◽  
Human Cervical Cancer

scholarly journals Punicalagin suppresses the proliferation and invasion of cervical cancer cells through inhibition of the β-catenin pathway

2017 ◽  
Vol 16 (2) ◽  
pp. 1439-1444 ◽  
Author(s):  
Jianming Tang ◽  
Bingshu Li ◽  
Shasha Hong ◽  
Cheng Liu ◽  
Jie Min ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Proliferation And Invasion

MicroRNA-142-3p inhibits cell proliferation and invasion of cervical cancer cells by targeting FZD7

Tumor Biology ◽  
2015 ◽  
Vol 36 (10) ◽  
pp. 8065-8073 ◽  
Author(s):  
Boya Deng ◽  
Yi Zhang ◽  
Siyang Zhang ◽  
Fang Wen ◽  
Yuan Miao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Proliferation And Invasion

scholarly journals LncRNA OTUD6B-AS1 Induces Cisplatin Resistance in Cervical Cancer Cells Through Up-Regulating Cyclin D2 via miR-206

2021 ◽  
Vol 11 ◽  
Author(s):  
Hui Hou ◽  
Rong Yu ◽  
Haiping Zhao ◽  
Hao Yang ◽  
Yuchong Hu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Luciferase Reporter ◽  
Cyclin D2 ◽  
Aberrant Expression ◽  
Qrt Pcr ◽  
Cervical Cancer Cells ◽  
Reporter Assays ◽  
Underlying Mechanisms

Cervical cancer is one of the most common gynecological cancers. Cisplatin resistance remains a major hurdle in the successful treatment of cervical cancer. Aberrant expression of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in cisplatin resistance. However, the regulatory functions of lncRNAs and miRNAs in cervical cancer cisplatin resistance and the underlying mechanisms are still elusive. Our qRT-PCR assays verified that miR-206 levels were down-regulated in cisplatin-resistant cervical cancer cells. The introduction of miR-206 sensitized cisplatin-resistant cervical cancer cells to cisplatin. Our qRT-PCR and luciferase reporter assays showed that Cyclin D2 (CCND2) was the direct target for miR-206 in cervical cancer cells. The cisplatin-resistant cervical cancer cells expressed higher CCND2 expression than the parental cells, whereas inhibition of CCND2 could sensitize the resistant cells to cisplatin treatment. Furthermore, we demonstrated that lncRNA OTUD6B-AS1 was up-regulated in cisplatin-resistant cervical cancer cells, and knocking down OTUD6B-AS1 expression induced re-acquirement of chemosensitivity to cisplatin in cervical cancer cells. We also showed that OTUD6B-AS1 up-regulated the expression of CCND2 by sponging miR-206. Low miR-206 and high OTUD6B-AS1 expression were associated with significantly poorer overall survival. Taken together, these results suggest that OTUD6B-AS1-mediated down-regulation of miR-206 increases CCND2 expression, leading to cisplatin resistance. Modulation of these molecules may be a therapeutic approach for cisplatin-resistant cervical cancer.

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