Silencing HMGN5 suppresses cell growth and promotes chemosensitivity in esophageal squamous cell carcinoma
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Updated: Feb 22, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Xiaoping Liu1, Weiping Ma1, Yanli Yan1
1Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, People's Republic of China.
Abstract:
Previous study has demonstrated that high mobility group nucleosome-binding domain 5 (HMGN5) is involved in tumorigenesis and the development of multidrug resistance in several human cancers. However, the role of HMGN5 in esophageal squamous cell carcinoma (ESCC) remains unclear. Here, we showed that HMGN5 was significantly upregulated in ESCC cells. Knockdown of HMGN5 significantly inhibited cell growth and induced cell apoptosis of ESCC cells. Moreover, knockdown of HMGN5 increased the sensitivity of ESCC cells towards cisplatin. By contrast, overexpression of HMGN5 showed the opposite effects. Further experiments demonstrated that HMGN5 regulated the expression of multidrug resistance 1, cyclin B1, and Bcl-2. Overall, our results reveal that HMGN5 promotes tumor progression of ESCC and is also an important regulator of chemoresistance. Our study suggests that inhibition of HMGN5 may be a potential strategy for improving effectiveness of ESCC treatment.
Insights
High mobility group nucleosome-binding domain 5 (HMGN5) promotes esophageal squamous cell carcinoma (ESCC) progression and chemoresistance. Inhibiting HMGN5 may enhance ESCC treatment effectiveness.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- High mobility group nucleosome-binding domain 5 (HMGN5) is implicated in tumorigenesis and multidrug resistance in various cancers.
- The specific role of HMGN5 in esophageal squamous cell carcinoma (ESCC) is not well-defined.
Purpose of the Study:
- To investigate the function of HMGN5 in ESCC.
- To determine the impact of HMGN5 on ESCC cell growth, apoptosis, and chemoresistance.
Main Methods:
- Quantitative analysis of HMGN5 expression in ESCC cells.
- HMGN5 knockdown and overexpression experiments in ESCC cell lines.
- Assessment of cell proliferation, apoptosis, and sensitivity to cisplatin.
- Analysis of key gene expression including multidrug resistance 1, cyclin B1, and Bcl-2.
Main Results:
- HMGN5 was significantly upregulated in ESCC cells.
- HMGN5 knockdown inhibited ESCC cell growth and induced apoptosis.
- Reduced HMGN5 expression increased sensitivity to cisplatin chemotherapy.
- HMGN5 overexpression yielded opposite effects, promoting tumor progression.
Conclusions:
- HMGN5 promotes tumor progression and chemoresistance in ESCC.
- HMGN5 is a potential therapeutic target for improving ESCC treatment outcomes.
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