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Updated: Nov 7, 2025
Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
HDAC2 enhances esophageal squamous cell carcinoma development through down-regulating microRNA-503-5p and promoting
Jindong Li1, Chengyan Jin1, Lihua Sun2
1Department of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China.
Objective:
Although esophageal squamous cell carcinoma (ESCC)-oriented mechanism has been widely explored, the integrated action of histone deacetylase 2 (HDAC2), microRNA (miR)-503-5p and C-X-C motif chemokine 10 (CXCL10) in ESCC has not been thoroughly explored. Thus, we performed the research to study the role of HDAC2/miR-503-5p/CXCL10 axis in ESCC.
Methods:
ESCC tissues and mucosal tissues (5 cm from cancer tissues) were collected, in which HDAC2, miR-503-5p and CXCL10 expression levels were tested. The mechanism of HDAC2, miR-503-5p and CXCL10 was interpreted. The viability, colony formation ability, apoptosis, invasion and migration abilities of ESCC cells were tested after HDAC2, miR-503-5p or CXCL10 expression was altered. Tumorigenesis in mice was observed to further verify the in vitro effects of HDAC2 and miR-503-5p.
Results:
HDAC2 and CXCL10 were up-regulated while miR-503-5p was down-regulated in ESCC. HDAC2 bound to miR-503-5p and miR-503-5p targeted CXCL10. Silencing HDAC2 or restoring miR-503-5p depressed viability, colony-forming, invasion and migration abilities and enhanced apoptosis of ESCC cells in vitro, as well as suppressed ESCC tumorigenesis in vivo. Inhibition of miR-503-5p or elevation of CXCL10 negated HDAC2 knockout-induced effects on ESCC cells.
Conclusion:
This work elucidates that HDAC2 knockdown retards the process of ESCC by elevating miR-503-5p and inhibiting CXCL10 expression, which may provide a guidance for ESCC management.
Insights
Histone deacetylase 2 (HDAC2) knockdown inhibits esophageal squamous cell carcinoma (ESCC) by increasing microRNA (miR)-503-5p and decreasing C-X-C motif chemokine 10 (CXCL10). This axis offers potential therapeutic strategies for ESCC management.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Esophageal squamous cell carcinoma (ESCC) mechanisms are under investigation.
- The specific roles of histone deacetylase 2 (HDAC2), microRNA (miR)-503-5p, and C-X-C motif chemokine 10 (CXCL10) in ESCC require further elucidation.
Purpose of the Study:
- To investigate the integrated action of the HDAC2/miR-503-5p/CXCL10 axis in ESCC.
- To determine the functional impact of this axis on ESCC cell behavior and tumorigenesis.
Main Methods:
- Analysis of HDAC2, miR-503-5p, and CXCL10 expression in ESCC tissues.
- In vitro assays assessing cell viability, colony formation, apoptosis, invasion, and migration following manipulation of HDAC2, miR-503-5p, or CXCL10.
- In vivo tumorigenesis studies in mice to validate in vitro findings.
Main Results:
- HDAC2 and CXCL10 were upregulated, while miR-503-5p was downregulated in ESCC.
- HDAC2 directly targets miR-503-5p, which in turn targets CXCL10.
- HDAC2 silencing or miR-503-5p restoration inhibited ESCC cell proliferation, migration, and invasion, while promoting apoptosis, both in vitro and in vivo.
- Conversely, miR-503-5p inhibition or CXCL10 upregulation counteracted the effects of HDAC2 knockdown.
Conclusions:
- HDAC2 knockdown suppresses ESCC progression by upregulating miR-503-5p and downregulating CXCL10.
- The HDAC2/miR-503-5p/CXCL10 axis represents a potential therapeutic target for managing ESCC.
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