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Published on: August 2, 2024
miR-29c-3p regulates proliferation and migration in ovarian cancer by targeting KIF4A
Songwei Feng1, Shanhui Luo1, Chenchen Ji2
1Department of Gynecology, The Second Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Background:
Increasing evidence suggested that microRNA and kinesin superfamily proteins play an essential role in ovarian cancer. The association between KIF4A and ovarian cancer (OC) was investigated in this study.
Methods:
We performed bioinformatics analysis in the GEO database to screen out the differentially expressed miRNAs (DEmiRNAs) associated with ovarian cancer prognosis. Upstream targeting prediction for KIF4A was acquired by using the mirDIP database. The potential regulatory factor miR-29c-3p for KIF4A was obtained from the intersection of the above all miRNAs. The prognosis of KIF4A and target-miRNA in OC was obtained in the subsequent analysis. qRT-PCR and Western blot detected KIF4A expression level in IOSE80 (human normal ovarian epithelial cell line). In the meantime, the gene expression level was detected in A2780, HO-8910PM, COC1, and SKOV3 cell lines (human ovarian carcinoma cell line). MTT and colony formation assays were used to detect cell proliferation of SKOV3 cell line. The following assays detected cell migration through the use of transwell and wound heal assays. Targeted binding relationship between KIF4A and miRNA was detected by using the dual-luciferase reporter assay.
Results:
Both high expression of KIF4A and lower expression of miR-29c-3p could be used as biomarkers indicating poor prognosis in OC patients. Cellular function tests confirmed that when KIF4A was silenced, it inhibited the proliferation and migration of OC cells. In addition, 3'-UTR of KIF4A had a direct binding site with miR-29c-3p, which indicated that the expression of KIF4A could be regulated by miR-29c-3p. In subsequent assays, the proliferation and migration of OC cells were inhibited by the overexpression of miR-29c-3p. At the same time, rescue experiments also confirmed that the promotion of KIF4A could be reversed by miR-29c-3p.
Conclusion:
In a word, our data revealed a new mechanism for the role of KIF4A in the occurrence and development of OC.
Insights
High KIF4A expression and low miR-29c-3p levels indicate poor ovarian cancer prognosis. MiR-29c-3p directly targets KIF4A, inhibiting ovarian cancer cell proliferation and migration, revealing a new regulatory mechanism.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs and kinesin superfamily proteins are implicated in ovarian cancer development.
- Investigating the specific role of KIF4A in ovarian cancer is crucial for understanding disease progression.
Purpose of the Study:
- To explore the association between KIF4A and ovarian cancer (OC).
- To identify potential microRNA regulators of KIF4A in OC.
- To elucidate the functional impact of the KIF4A-miR-29c-3p interaction on OC progression.
Main Methods:
- Bioinformatics analysis of the GEO database to identify prognostic microRNAs in OC.
- Utilized mirDIP database for upstream targeting prediction of KIF4A.
- Validated KIF4A and miR-29c-3p expression via qRT-PCR and Western blot.
- Assessed OC cell proliferation, migration, and invasion using MTT, colony formation, Transwell, and wound healing assays.
- Dual-luciferase reporter assay confirmed the direct binding between KIF4A and miR-29c-3p.
Main Results:
- High KIF4A expression and low miR-29c-3p expression correlate with poor prognosis in OC patients.
- Silencing KIF4A significantly inhibited proliferation and migration of OC cells.
- MiR-29c-3p directly binds to the 3'-UTR of KIF4A, regulating its expression.
- Overexpression of miR-29c-3p suppressed OC cell proliferation and migration, with rescue experiments confirming KIF4A's role.
Conclusions:
- KIF4A acts as an oncogene in ovarian cancer.
- MiR-29c-3p functions as a tumor suppressor by targeting KIF4A in OC.
- This study reveals a novel regulatory mechanism involving KIF4A and miR-29c-3p in ovarian cancer pathogenesis.
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