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FoxM1 promotes the migration of ovarian cancer cell through KRT5 and KRT7
Ziyu Zhang1, Kaijia Tu2, Faying Liu1
1Key Laboratory of Women's Reproductive Health of Jiangxi, Jiangxi Maternal and Child Health Hospital, Nanchang, Jiangxi 330006, PR China; Central Laboratory, Jiangxi Maternal and Child Health Hospital, Nanchang, Jiangxi 330006, PR China.
Abstract:
Forkhead box M1(FoxM1) played an important role in the pathogenesis of ovarian cancer, but its downstream molecular network is mysterious. Here, we combined ChIP-seq with RNA-seq analysis and identified 687 FoxM1-binding regions and 182 genes regulated by FoxM1. The above data pointed out that KRT5 and KRT7 were downstream target genes of FoxM1. Next, we used qPCR and Western blot to verify that FoxM1 knockdown inhibited the expression levels of KRT5 and KRT7. We also demonstrated that FoxM1 regulated KRT5 and KRT7 genes expression through binding a consensus AP-2 cis element, and showed that KRT5 and KRT7 deficiency could prevent the migration but not proliferation of SK-OV-3 cells. Finally, tissue microarray results indicated that KRT5 and KRT7 were highly expressed in ovarian cancer and positively correlated with FoxM1 expression. TCGA database showed that high expression of KRT5 and KRT7 could significantly reduce the survival rate of patients with ovarian cancer. The above results clarify the specific downstream molecular network of FoxM1 to promote the pathogenesis of ovarian cancer, and provide a basis experiment for the judgment of ovarian cancer prognosis and the design of drug targets.
Insights
Forkhead box M1 (FoxM1) promotes ovarian cancer by regulating keratin genes KRT5 and KRT7. Targeting this pathway may offer new strategies for ovarian cancer treatment and prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Forkhead box M1 (FoxM1) is implicated in ovarian cancer pathogenesis.
- The precise downstream molecular mechanisms of FoxM1 in this context remain unclear.
Purpose of the Study:
- To elucidate the downstream molecular targets and network of FoxM1 in ovarian cancer.
- To investigate the role of FoxM1-regulated genes in ovarian cancer progression and patient survival.
Main Methods:
- ChIP-seq and RNA-seq analyses were employed to identify FoxM1 targets.
- Quantitative PCR (qPCR) and Western blotting validated gene expression changes.
- Cell migration and proliferation assays were performed.
- Tissue microarrays and TCGA database analysis assessed clinical relevance.
Main Results:
- Identified 687 FoxM1-binding regions and 182 FoxM1-regulated genes, including KRT5 and KRT7.
- FoxM1 knockdown decreased KRT5 and KRT7 expression, mediated by binding to an AP-2 cis element.
- KRT5 and KRT7 deficiency inhibited SK-OV-3 cell migration but not proliferation.
- High KRT5 and KRT7 expression in ovarian tumors correlated with FoxM1 and reduced patient survival.
Conclusions:
- FoxM1 promotes ovarian cancer pathogenesis by regulating KRT5 and KRT7.
- KRT5 and KRT7 are potential prognostic biomarkers and therapeutic targets for ovarian cancer.
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