The ESR1-MYH14 axis functions as a critical driver of cervical cancer progression and metastasis

BACKGROUND: Cervical cancer remains a major cause of cancer-related mortality in women, yet its molecular mechanisms of progression and metastasis are not fully defined. This study explores the oncogenic role of the ESR1 (estrogen receptor α)-MYH14 (myosin heavy chain 14) signaling axis in cervical cancer. METHODS: Quantitative real-time PCR and Western blotting were used to assess RNA and protein levels. The transcriptional regulation of MYH14 by ESR1 was verified through chromatin immunoprecipitation quantitative PCR and dual-luciferase assays. Cellular proliferation, migration, and invasion were evaluated using CCK-8, colony formation, wound healing, and transwell assays. Xenograft and tail vein metastasis models were applied to examine the effects of MYH14 silencing and ESR1 inhibition by AZD9833. RESULTS: MYH14 was markedly upregulated in cervical cancer tissues and correlated with poor prognosis. MYH14 knockdown suppressed proliferation and metastasis both in vitro and in vivo. ESR1 functioned as a transcriptional activator of MYH14, enhancing c-Myc and MMP9 expression, whereas MYH14 silencing or AZD9833 treatment reversed these oncogenic effects and reduced ESR1, MYH14, c-Myc, and MMP9 levels. CONCLUSION: The ESR1-MYH14 signaling axis drives cervical cancer growth and metastasis. Targeting this pathway may represent a promising therapeutic strategy for cervical cancer management.