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Role of ZNF334 in cervical cancer: implications for EMT reversal and tumor suppression
Qian Li1,2, Xiangyi Zhou1, Jiayi Xiao3
1Department of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Abstract:
Zinc-finger proteins are involved in many biological processes. However, the role of Zinc-finger protein 334 (ZNF334) in cervical cancer remains unidentified. This study showed that promoter methylation of ZNF334 was responsible for its reduced expression. ZNF334 suppressed malignant biological behaviors in cervical cancer. Notably, ZNF334 reversed the EMT process both in vitro and in vivo. RNA-seq coupled with bioinformatics analysis caught P3H3 which is upregulated by ZNF334. Dual-luciferase reporter and Chromatin immunoprecipitation assays illustrated that ZNF334 directly regulate P3H3. Knockdown of P3H3 attenuated the reversal of EMT induced by ZNF334. Additionally, ZNF334 overexpression sensitized cervical cancer cells to the cytotoxic effects of paclitaxel, cyclosporine and sunitinib. In conclusions, this study illustrated that DNA methylation-based silencing ZNF334 played a vital role in cervical cancer, by regulating P3H3 in turn affects EMT. ZNF334 has the potential to become a novel diagnostic biomarker and a potential treatment target for cervical cancer.
Insights
Reduced expression of Zinc-finger protein 334 (ZNF334) due to DNA methylation promotes cervical cancer progression. ZNF334 suppresses malignant behaviors by regulating P3H3 and reversing EMT, offering potential as a diagnostic biomarker and therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Zinc-finger proteins (ZFPs) are crucial in various biological functions.
- The specific role of Zinc-finger protein 334 (ZNF334) in cervical cancer pathogenesis is largely unknown.
- Understanding ZNF334's function could reveal new therapeutic strategies for cervical cancer.
Purpose of the Study:
- To investigate the role of ZNF334 in cervical cancer.
- To elucidate the molecular mechanisms underlying ZNF334's function in cervical cancer.
- To evaluate ZNF334 as a potential diagnostic biomarker and therapeutic target.
Main Methods:
- Analysis of ZNF334 promoter methylation and expression levels in cervical cancer.
- In vitro and in vivo experiments to assess ZNF334's effect on malignant behaviors and epithelial-mesenchymal transition (EMT).
- RNA sequencing, dual-luciferase reporter assays, and chromatin immunoprecipitation to identify and validate ZNF334 targets, including P3H3.
Main Results:
- Promoter methylation significantly reduced ZNF334 expression in cervical cancer.
- ZNF334 suppressed cervical cancer cell proliferation, migration, and invasion, and reversed EMT.
- ZNF334 directly upregulates P3H3 expression, and P3H3 knockdown abrogated ZNF334-mediated EMT reversal.
- ZNF334 overexpression enhanced sensitivity to paclitaxel, cyclosporine, and sunitinib.
Conclusions:
- DNA methylation-mediated silencing of ZNF334 is a key factor in cervical cancer progression.
- ZNF334 exerts its tumor-suppressive effects by regulating P3H3 and consequently influencing EMT.
- ZNF334 demonstrates potential as a novel diagnostic biomarker and therapeutic target for cervical cancer.
