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Background <p>Prostate cancer (PCa) recurrence, progression, and drug resistance remain critical clinical challenges. Bioinformatics analyses have implicated ZNF692 in PCa initiation and progression. This study aimed to investigate its impact on PCa biological behavior and underlying mechanisms, potentially identifying novel diagnostic and therapeutic targets.</p> Methods <p>ZNF692 protein expression was detected in 75 paired PCa and adjacent normal tissues using immunohistochemical (IHC) SP staining, and its correlation with clinicopathological features was analyzed. RT-qPCR and Western blot (WB) were used to detect the expression of ZNF692 mRNA and protein in 5 PCa cell lines (PC3, DU145, LNCaP, 22RV1, C4-2) and normal prostate cell line (RWPE-1). ZNF692 knockdown and overexpression PCa cell lines were established by lentivirus transfection. Cell proliferation, migration and invasion abilities were detected by CCK-8, Colony Formation Assay, Scratch assay and Transwell assay; in vivo effects were verified by nude mouse subcutaneous tumor formation and tail vein lung metastasis models. Differentially expressed proteins were screened by proteomics sequencing, and pathway enrichment was analyzed by Kyoto Encyclopedia of Genes and Genomes (KEGG); WB was used to verify the effect of ZNF692 on the core and downstream proteins of The nuclear factor-kappa B (NF-κB) signaling pathway; functional recovery experiments (LPS activator/SN50 inhibitor) confirmed the pathway dependence.</p> Results <p>ZNF692 was highly expressed in prostate cancer tissues and was positively correlated with the clinical pathological stage. The expression of ZNF692 mRNA and protein in prostate cancer cell lines was significantly increased. Overexpression of ZNF692 promotes the proliferation, migration and invasion of prostate cancer cells, while knockdown inhibits them; in vivo experiments also confirmed its tumor-promoting effect. Proteomic sequencing identified 1109 differentially expressed proteins, and KEGG analysis showed that the NF-κB signaling pathway-a classic cancer-related pathway-was significantly enriched. WB confirmed that ZNF692 can activate the core and downstream proteins of the NF-κB signaling pathway. Functional restoration experiments demonstrated that ZNF692 functions through the NF-κB pathway (LPS can partially restore the inhibitory effect of knocking down ZNF692, and SN50 can partially reverse the promoting effect of overexpressing ZNF692).</p> Conclusion <p>ZNF692 may promote cell proliferation, migration and invasion of prostate cancer cells by activating the NF-κB signaling pathway.</p>

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ZNF692 promotes the proliferation, invasion and migration of prostate cancer cells by activating the NF-κB signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月4日

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  • Hanmin Chen,
  • Gengqing Wu,
  • Qingming Zeng,
  • Jiedong Zhou,
  • Li Yu,
  • Xiaofeng Zou,
  • Guoxi Zhang,
  • Yuhua Zou

摘要

Background

Prostate cancer (PCa) recurrence, progression, and drug resistance remain critical clinical challenges. Bioinformatics analyses have implicated ZNF692 in PCa initiation and progression. This study aimed to investigate its impact on PCa biological behavior and underlying mechanisms, potentially identifying novel diagnostic and therapeutic targets.

Methods

ZNF692 protein expression was detected in 75 paired PCa and adjacent normal tissues using immunohistochemical (IHC) SP staining, and its correlation with clinicopathological features was analyzed. RT-qPCR and Western blot (WB) were used to detect the expression of ZNF692 mRNA and protein in 5 PCa cell lines (PC3, DU145, LNCaP, 22RV1, C4-2) and normal prostate cell line (RWPE-1). ZNF692 knockdown and overexpression PCa cell lines were established by lentivirus transfection. Cell proliferation, migration and invasion abilities were detected by CCK-8, Colony Formation Assay, Scratch assay and Transwell assay; in vivo effects were verified by nude mouse subcutaneous tumor formation and tail vein lung metastasis models. Differentially expressed proteins were screened by proteomics sequencing, and pathway enrichment was analyzed by Kyoto Encyclopedia of Genes and Genomes (KEGG); WB was used to verify the effect of ZNF692 on the core and downstream proteins of The nuclear factor-kappa B (NF-κB) signaling pathway; functional recovery experiments (LPS activator/SN50 inhibitor) confirmed the pathway dependence.

Results

ZNF692 was highly expressed in prostate cancer tissues and was positively correlated with the clinical pathological stage. The expression of ZNF692 mRNA and protein in prostate cancer cell lines was significantly increased. Overexpression of ZNF692 promotes the proliferation, migration and invasion of prostate cancer cells, while knockdown inhibits them; in vivo experiments also confirmed its tumor-promoting effect. Proteomic sequencing identified 1109 differentially expressed proteins, and KEGG analysis showed that the NF-κB signaling pathway-a classic cancer-related pathway-was significantly enriched. WB confirmed that ZNF692 can activate the core and downstream proteins of the NF-κB signaling pathway. Functional restoration experiments demonstrated that ZNF692 functions through the NF-κB pathway (LPS can partially restore the inhibitory effect of knocking down ZNF692, and SN50 can partially reverse the promoting effect of overexpressing ZNF692).

Conclusion

ZNF692 may promote cell proliferation, migration and invasion of prostate cancer cells by activating the NF-κB signaling pathway.