HDAC10 Inhibits Cervical Cancer Progression through Downregulating the HDAC10-microRNA-223-EPB41L3 Axis

Yuan Yuan Gu1,2,3, Guan Nan Zhou1,2, Yao Li4

  • 1Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai 200011, China.

Journal of Oncology
|January 25, 2022
PubMed
Abstract

Insights

Histone deacetylase 10 (HDAC10) inhibits cervical cancer (CC) by reducing microRNA-223 (miR-223) and EPB41L3. This finding offers new insights for managing CC and precancerous lesions.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Cervical cancer (CC) tumorigenesis is studied, but the roles of histone deacetylase 10 (HDAC10), microRNA, and downstream pathways remain unclear.
  • Investigating the molecular mechanisms of HDAC10, miR-223, and EPB41L3 in CC is crucial for understanding disease progression.

Purpose of the Study:

  • To determine the expression levels of HDAC10, miR-223, and EPB41L3 in cervical cancer, precancerous lesions, and normal tissues.
  • To elucidate the regulatory network involving HDAC10, miR-223, and EPB41L3 in cervical cancer cells.

Main Methods:

  • Tissue collection: cervical cancer, precancerous lesions, and normal cervical tissues.
  • Expression analysis of HDAC10, miR-223, and EPB41L3.
  • Functional studies involving alteration of HDAC10, miR-223, or EPB41L3 expression in cervical cancer cells.

Main Results:

  • HDAC10 expression was reduced in cervical cancer and precancerous lesions.
  • miR-223 expression was elevated in cervical cancer tissues.
  • HDAC10 directly interacts with miR-223, which in turn targets EPB41L3. HDAC10 suppresses CC invasion and tumorigenesis by downregulating miR-223 and EPB41L3.

Conclusions:

  • HDAC10 acts as a tumor suppressor in cervical cancer by inhibiting the miR-223/EPB41L3 pathway.
  • This regulatory axis provides a potential therapeutic target for cervical cancer and precancerous lesions.

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