Dataset Information

MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin.

ABSTRACT:

Background

MicroRNA-217 (miR-217) has been demonstrated to participate in the tumorigenesis and progression of various types of cancers. Nevertheless, the role of miR-217 in cervical carcinoma still remains not fully elucidated. This current work sought to investigate the role of miR-217 in the growth, migration, and invasion of cervical carcinoma and detect the role of miR-217 in the chemosensitivity of cervical carcinoma cell to cisplatin.

Materials and methods

The levels of miR-217 in 65 pairs of cervical carcinoma tissues and matched normal tissues were detected using quantitative real-time-PCR assay. The roles of miR-217 on the growth, apoptosis, migration, and invasion of cervical cancer SiHa and Ca-Ski cells were analyzed using Cell Counting Kit-8, flow cytometry, wound healing, and Transwell invasion assays, respectively. The target of miR-217 was identified using the online analysis tool TargetScan (http://www.targetscan.org/vert_72/) and was verified by luciferase reporter and immunoblotting assays. The xenograft tumor model was constructed to explore the impact of miR-217 on the growth of cervical carcinoma cell in vivo.

Results

The level of miR-217 was remarkably lower in cervical carcinoma tissues than that in noncancerous tissues. Overregulation of miR-217 markedly suppressed the aggressiveness of cervical cancer cell and induced cell apoptosis through regulating V-Ki-Ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS). Finally, upregulation of miR-217 enhanced the chemosensitivity of both SiHa and Ca-Ski cervical cancer cells toward cisplatin.

Conclusion

Altogether, upregulation of miR-217 inhibits the aggressiveness phenotypes of cervical carcinoma cell via regulating KRAS gene and increases the sensitivity of cervical cancer cell to cisplatin.

SUBMITTER: Yin Z

PROVIDER: S-EPMC6352857 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin.

Yin Zhaojun Z Ren Weiru W

OncoTargets and therapy 20190123

<h4>Background</h4>MicroRNA-217 (miR-217) has been demonstrated to participate in the tumorigenesis and progression of various types of cancers. Nevertheless, the role of miR-217 in cervical carcinoma still remains not fully elucidated. This current work sought to investigate the role of miR-217 in the growth, migration, and invasion of cervical carcinoma and detect the role of miR-217 in the chemosensitivity of cervical carcinoma cell to cisplatin.<h4>Materials and methods</h4>The levels of miR ...[more]

PMID: 30774364

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Project description:BackgroundTo study miR-30b-5p expression in esophageal squamous cell carcinoma (ESCC) by comparisons between tumor tissues and matched adjacent non-cancerous tissues to elucidate the correlation between miR-30b-5p expression and ESCC clinical parameters, and to explore the signaling pathways associated with miR-30b-5p and key target genes.MethodsClinical data, cancer tissues, and adjacent non-cancerous tissues of 32 patients diagnosed with ESCC were collected from Taizhou Hospital of Zhejiang Province. The expression levels of miR-30b-5p were determined by real-time polymerase chain reaction (RT-PCR). mRNA data for ESCC tissues and normal tissues, and clinical materials of patients with ESCC were obtained from the Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA). Associations between miR-30b-5p expression and clinical features of patients with ESCC and overall survival were explored. A bioinformatics analysis was performed to determine the pathways and key miR-30b-5p targets associated with ESCC. Additionally, a cytological experiment was performed to evaluate the biological functions of miR-30b-5p. Finally, correlations between miR-30b-5p and key targets involved in PI3K/Akt signaling pathways were validated by western blotting.ResultsThe expression level of miR-30b-5p in the 32 ESCC tissues was significantly lower than that in adjacent normal tissues (P<0.01) and was significantly disparate in the T stage, with higher expression in T1 than in T2 (P<0.05). Among the patients with higher expression levels of miR-30b-5p in ESCC tissues than in adjacent normal tissues, patients with higher expression of miR-30b-5p had a better prognosis (P<0.05). An analysis of gene chip data from the GEO database showed similar results. A gene enrichment analysis indicated a series of pathways that may be associated with the downregulation of miR-30b-5p, including focal adhesion, ECM-receptor interaction, and PI3K/Akt signaling pathways. Seven key target genes (PDGFRB, VIM, ITGA5, ACTN1, THBS2, SERPINE1, and RUNX2) were identified; these were found to be upregulated in ESCC tissues and were negatively correlated with miR-30b-5p. Functional experiments showed that miR-30b-5p attenuated migration (P<0.01) and invasion (P<0.05) in the Eca109 cell line. Moreover, the levels of ITGA5, PDGFRB, p-PI3K, and p-AKT, which are involved in the PI3K/Akt signaling pathway, were decreased in the miR-30b-5p-overexpressing Eca109 cell line.ConclusionsUpregulated miR-30b-5p may inhibit migration and invasion in ESCC by targeting ITGA5, PDGFRB, and signaling pathways, such as PI3K/Akt, involved in ESCC regulation. Our results indicate that miR-30b-5p plays an important role in the occurrence and progression of ESCC and is a potential therapeutic target.

Dataset Information

MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin.

Background

Materials and methods

Results

Conclusion

Publications

MicroRNA-217 acts as a tumor suppressor and correlates with the chemoresistance of cervical carcinoma to cisplatin.

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