miR-187 inhibits the growth of cervical cancer cells by targeting FGF9

Liu, Hua; Luo, Renshi; Chen, Xiaoqi; Zhao, Yong; Tan, Aili

doi:10.3892/or.2017.5916

Cited by 42 publications

(37 citation statements)

References 23 publications

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“…Several studies have confirmed that miRNAs are closely related to tumor development and can be used as potential diagnostic or therapeutic targets for tumors (Rupaimoole et al, 2016), including CC (Banno et al, 2014). For example, miR-197 could promote the proliferation of CC cells by targeting FGF9 (Liang et al, 2017). Overexpression of miR-214 could inhibit the migration and invasion of CC cells by regulating ARL2 (Peng et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

LncRNA TUSC8 inhibits the invasion and migration of cervical cancer cells via miR‐641/PTEN axis

Zhu

Liu

Zhang

et al. 2019

Cell Biology International

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Cervical cancer (CC) is the fourth leading cause of cancer‐related death in women worldwide. There is an urgent need to find novel targets for the treatment of CC. Recently, microRNA have emerged as critical factors in tumorigenesis. In this study, we aimed to investigate the mechanism of miR‐641 on the migration and invasion of CC cells. In silico analysis revealed putative interaction between miR‐641 and phosphatase and tensin homolog (PTEN) RNA/lncRNA tumor suppressor candidate 8 (TUSC8). Hence we evaluated the expression of TUSC8, miR‐641, and PTEN. We found that the expressions of TUSC8 and PTEN were decreased in CC tissues, whereas miR‐641 expression was increased. Inhibition of miR‐641 suppressed the migration and invasion of Hela cells. In addition, TUSC8 and PTEN were upstream and downstream target molecule of miR‐641, respectively. Overexpression of TUSC8 promoted PTEN expression, and suppressed the invasion and migration of Hela cells, whereas miR‐641 mimic treatment changed the effects. These results demonstrated that overexpression of TUSC8 could inhibit the invasion and migration of CC cells by upregulating PTEN via miR‐641.

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Section: Introductionmentioning

confidence: 99%

LncRNA TUSC8 inhibits the invasion and migration of cervical cancer cells via miR‐641/PTEN axis

Zhu

Liu

Zhang

et al. 2019

Cell Biology International

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“…Nevertheless, the outcome of current therapy strategies is still poor. Therefore, investigating the exact molecular mechanisms of CC may promote the identification of novel biomarkers and treatment targets, which is critical for improving the prognosis of these patients [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

SKA3 promotes cell proliferation and migration in cervical cancer by activating the PI3K/Akt signaling pathway

Wang

Niu

et al. 2018

Cancer Cell Int

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BackgroundCervical cancer (CC) is one of the most common cancers among females worldwide. Spindle and kinetochore-associated complex subunit 3 (SKA3), located on chromosome 13q, was identified as a novel gene involved in promoting malignant transformation in cancers. However, the function and underlying mechanisms of SKA3 in CC remain unknown. Using the Oncomine database, we found that expression of SKA3 mRNA is higher in CC tissues than in normal tissues and is linked with poor prognosis.MethodsIn our study, immunohistochemistry showed increased expression of SKA3 in CC tissues. The effect of SKA3 on cell proliferation and migration was evaluated by CCK8, clone formation, Transwell and wound-healing assays in HeLa and SiHa cells with stable SKA3 overexpression and knockdown. In addition, we established a xenograft tumor model in vivo.ResultsSKA3 overexpression promoted cell proliferation and migration and accelerated tumor growth. We further identified that SKA3 is involved in regulating cell cycle progression and the PI3K/Akt signaling pathway via RNA-sequencing (RNA-Seq) and gene set enrichment analyses. Western blotting results revealed that SKA3 overexpression increased levels of p-Akt, cyclin E2, CDK2, cyclin D1, CDK4, E2F1 and p-Rb in HeLa cells. Additionally, the use of an Akt inhibitor (GSK690693) significantly reversed the cell proliferation capacity induced by SKA3 overexpression in HeLa cells.ConclusionsWe suggest that SKA3 overexpression contributes to CC cell growth and migration by promoting cell cycle progression and activating the PI3K–Akt signaling pathway, which may provide potential novel therapeutic targets for CC treatment.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0670-4) contains supplementary material, which is available to authorized users.

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“…14 Liang et al indicated that miR-187 inhibited the proliferation and promoted apoptosis of CC cells, at least partly through repression of the fibroblast growth factor 9 (FGF9) expression. 15 Moreover, Hua et al demonstrated that miR-338-3p suppressed CC cell proliferation and induced apoptosis via downregulating target gene metastasis-associated in colon cancer-1 (MACC1) through mitogen-activated protein kinase (MAPK) signaling pathway. 16 MiR-499a-5p has gained increasing attention in cancer research because of its anti-tumor action.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-499a-5p Inhibits Pr5/4/20 publish l Cancer Cells via Targeting eIF4E</p>

Gu¹,

Ma²,

Liu³

et al. 2020

OTT

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Introduction: The present study aimed to explore the role of miR-499a-5p and its molecular mechanism in cervical cancer (CC). Methods: Quantitative real-time PCR (QRT-PCR) and Western blotting were performed to detect the expression of miR-499a-5p and eukaryotic translation initiation factor 4E (eIF4E) in CC tissues and cell lines. The proliferation, migration, and invasion of CC cells were detected by MTT assay, wound healing assay, and Transwell assay. Apoptosis was evaluated by flow cytometry and alterations of apoptosis-related genes. The effect of miR-499a-5p on epithelial-mesenchymal transition (EMT) was examined by determining the protein levels of EMT-associated genes. Then, colony formation assay was used to determine the radiosensitivity of CC cells. A dualluciferase reporter assay was performed to confirm the direct target of miR-499a-5p. Results: MiR-499a-5p was significantly downregulated in CC tissues and cell lines. Overexpression of miR-499a-5p or eIF4E knockdown markedly inhibited cell proliferation, invasion, migration, and EMT, and enhanced apoptosis. eIF4E was predicted and verified as a target gene of miR-499a-5p. The influence of miR-499a-5p upregulation on proliferation, apoptosis, invasion, migration, EMT, and radiosensitivity was abrogated by eIF4E overexpression. Discussion: MiR-499a-5p promoted the apoptosis and radiosensitivity and inhibited proliferation, invasion, migration, and EMT by directly targeting eIF4E in CC cells.

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miR-187 inhibits the growth of cervical cancer cells by targeting FGF9

Cited by 42 publications

References 23 publications

LncRNA TUSC8 inhibits the invasion and migration of cervical cancer cells via miR‐641/PTEN axis

LncRNA TUSC8 inhibits the invasion and migration of cervical cancer cells via miR‐641/PTEN axis

SKA3 promotes cell proliferation and migration in cervical cancer by activating the PI3K/Akt signaling pathway

<p>MiR-499a-5p Inhibits Pr5/4/20 publish l Cancer Cells via Targeting eIF4E</p>

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