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

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.

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.

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.

The ESR1-MYH14 signaling axis drives cervical cancer growth and metastasis. Targeting this pathway may represent a promising therapeutic strategy for cervical cancer management.