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Updated: Oct 5, 2025

Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
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.
Background:
Although the tumorigenesis of cervical cancer (CC) has been widely investigated and recognized, the study of the systematic impact of histone deacetylase 10 (HDAC10), microRNA, and downstream molecular mechanisms in CC is still limited. Herein, cervical cancer, precancer lesions, and normal cervical tissues were collected to test the expression level of HDAC10, miR-223, and EPB41L3. The mechanism of HDAC10, miR-223, and EPB41L3 was interpreted in cervical cancer cells after HDAC10, miR-223, or EPB41L3 expression was altered.
Results:
HDAC10 was poorly expressed in cervical cancer and precancer lesions, while miR-223 was highly expressed in cervical cancer. HDAC10 bound to miR-223, and miR-223 targeted EPB41L3. HDAC10 depressed the invasion property and tumorigenesis of cervical cancer via downregulating miR-223 and subsequently targeting EPB41L3.
Conclusion:
The study clarifies that HDAC10 inhibits cervical cancer by downregulating miR-223 and subsequently targeting EPB41L3 expression, which might provide a new insight for management upon cervical cancer and precancer lesions.
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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