Clinical value of survivin and its underlying mechanism in ovarian cancer: A bioinformatics study based on GEO and TCGA data mining

Li, Xiao‐Jiao; Pang, Jin‐Shu; Li, Yaomei; Ahmed, Farah Abdirahman; He, Rong‐Quan; Ma, Jie; Ma, Fuchao; Chen, Gang

doi:10.1016/j.prp.2017.12.020

Cited by 14 publications

(10 citation statements)

References 27 publications

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“…After browsing the Gene Expression Pro ling Interactive Analysis (GEPIA) database (http://gepia.cancerpku.cn/help.html) website [14], we discovered that MSC-AS1 expression in ovarian cancer tissues was remarkably lower than that in normal tissues, as exhibited in Fig. 1A B. Consistently, qRT-PCR assay showed that the expression level of MSC-AS1 was markedly lower in ovarian cancer tissues comparison with that in adjacent non-tumor tissues (Fig.…”

Section: Msc-as1 Expression Was Reduced In Ovarian Cancer Tissues Andmentioning

confidence: 99%

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LncRNA-MSC-AS1 inhibits the ovarian cancer progression by targeting miR-425-5p

Zhao

Yuan

Zhu

et al. 2021

Preprint

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Background Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) were reported to be aberrantly expressed and related to the pathogenesis of ovarian cancer. However, the role and regulatory mechanism of MSC-AS1 in ovarian cancer has yet to be fully elucidated. Methods Expression of lncRNA MSC-AS1 (MSC-AS1) and microRNA-425-5p (miR-425-5p) in the ovarian cancer tissue samples and cell lines was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The functions of MSC-AS1 on ovarian cancer cell proliferation, cell cycle and apoptosis were determined using MTT, colony formation and flow cytometry analyses. The protein expression levels were evaluated using western blot assay. The targeting relationship MSC-AS1 and miR-425-5p was verified via dual-luciferase reporter assay. Results MSC-AS1 expression level was lowly expressed, while miR-425-5p level was highly in ovarian cancer tissues and cells. Elevation of MSC-AS1 has the ability to significantly inhibit cell proliferation and facilitate cell apoptosis in SKOV3 cells. Moreover, MSC-AS1 targeted and negatively modulated miR-425-5p. MiR-425-5p up-regulation has been proved to partially reverse the tumor suppressive function of MSC-AS1 overexpression. Conclusion MSC-AS1 sponged miR-425-5p to inhibit the ovarian cancer progression. These findings may provide a promising therapeutic target for the treatment of ovarian cancer.

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Section: Msc-as1 Expression Was Reduced In Ovarian Cancer Tissues Andmentioning

confidence: 99%

Section: Msc-as1 Expression Was Reduced In Ovarian Cancer Tissues Andmentioning

confidence: 99%

LncRNA-MSC-AS1 inhibits the ovarian cancer progression by targeting miR-425-5p

Zhao

Yuan

Zhu

et al. 2021

Preprint

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“…Survivin (BIRC5) is the smallest member of the inhibitors of apoptosis protein (IAP) family, and found to be highly expressed in a variety of human cancers, including breast cancer and ovarian cancer, but low expression of survivin was observed in adult normal tissues (21)(22)(23)(24). Survivin expression is well-correlated with tumor metastasis and chemoresistance in several cancer types, such as melanoma, renal, prostate, breast (25)(26)(27)(28), and ovarian (10,(29)(30)(31)(32).…”

Section: Introductionmentioning

confidence: 99%

Ovarian Primary and Metastatic Tumors Suppressed by Survivin Knockout or a Novel Survivin Inhibitor

Zhao

Wang

et al. 2019

Molecular Cancer Therapeutics

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Survivin, a member of the inhibitor of apoptosis family, is upregulated in multiple cancers including ovarian cancer, but is rarely detectable in normal tissues. We previously reported that survivin promoted epithelial-to-mesenchymal transition (EMT) in ovarian cancer cells, suggesting that survivin may contribute to ovarian tumor metastasis and chemoresistance. In this study, we tested whether knockout or pharmacologic inhibition of survivin overcomes chemoresistance and suppresses tumor metastasis. The genetic loss of survivin suppressed tumor metastasis in an orthotopic ovarian cancer mouse model. To pharmacologically test the role of survivin on ovarian tumor metastasis, we treated chemo-resistant ovarian cancer cells with a selective survivin inhibitor, MX106, and found that MX106 effectively overcame chemoresistance in vitro. MX106 inhibited cell migration and invasion by attenuating the TGFb pathway and inhibiting EMT in ovarian cancer cells. To evaluate the efficacy of MX106 in inhibiting ovarian tumor metastasis, we treated an orthotopic ovarian cancer mouse model with MX106, and found that MX106 efficiently inhibited primary tumor growth in ovaries and metastasis in multiple peritoneal organs as compared with vehicle-treated control mice. Our data demonstrate that inhibition of survivin using either genetic knockout or a novel inhibitor MX106 suppresses primary ovarian tumor growth and metastasis, supporting that targeting survivin could be an effective therapeutic approach in ovarian cancer.

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“…Meanwhile, in the past decade, the research to small interfering RNAs (siRNAs) as an emerging therapy and one kind of drugs to treat diseases especially neoplasms has become more and more deep and meaningful. 11,12 Considering the survivin protein may be against the death of cells, [13][14][15] we try to combine Pt(IV) with siRNA of survivin to enhance antitumor effect. Furthermore, in recent years, due to the unique physical and chemical properties of the nanoparticles, such as: good controllability, going through the biological barrier, improving the target property through the enhanced permeability and retention (EPR) effect, the nanoparticles has opened an new eld of treating diseases especially tumors.…”

Section: Introductionmentioning

confidence: 99%