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Updated: Apr 8, 2026

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Published on: July 22, 2020
HDAC5 promotes colorectal cancer cell proliferation by up-regulating DLL4 expression
Ping He1, Jiexiong Liang1, Tiansong Shao1
1Department of General Surgery, Bejing Anzhen Hospital, Capital Medical University Beijing, China.
Abstract:
The histone deacetylase (HDACs) family contains a family of enzymes, which are involved in modulating a wide range of cellular processes, such as proliferation, differentiation, apoptosis, and cell cycle progression. However, the biological function of HDAC5 in colorectal cancer has not been well established. In the current research, our data showed that the mRNA and protein levels of HDAC5 were up-regulated in human colorectal cancer cell lines. CCK-8 assay showed that overexpression of HDAC5 significantly promoted the proliferation of colorectal cancer cell lines including SW480 and HCT116. On the contrary, HDAC5 knockdown using small interfering RNA suppressed cell growth in colorectal tumor cells. At the molecular level, we demonstrated that HDAC5 promoted the expression of DLL4. In addition, down-regulation of DLL4 diminished the proliferative effects of HDAC5 in human colorectal cancer cells. Taken together, these results suggest that HDAC5 elevates the proliferation of colorectal cancer cells through up-regulation of DLL4. The current study might provide novel potential therapeutic targets in the treatment of colorectal cancer.
Insights
Histone deacetylase 5 (HDAC5) promotes colorectal cancer cell proliferation by increasing DLL4 expression. This study identifies HDAC5 as a potential therapeutic target for colorectal cancer treatment.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Histone deacetylases (HDACs) regulate critical cellular processes.
- The specific role of HDAC5 in colorectal cancer (CRC) remains unclear.
- Understanding HDAC5's function is crucial for developing novel CRC therapies.
Purpose of the Study:
- To investigate the role of HDAC5 in colorectal cancer.
- To elucidate the molecular mechanism by which HDAC5 affects CRC cell proliferation.
- To identify potential therapeutic targets for CRC.
Main Methods:
- Analysis of HDAC5 mRNA and protein levels in CRC cell lines.
- Cell proliferation assays (CCK-8) following HDAC5 overexpression and knockdown (siRNA).
- Investigation of the relationship between HDAC5 and DLL4 expression.
Main Results:
- HDAC5 expression is upregulated in human colorectal cancer cell lines.
- Overexpression of HDAC5 significantly promotes CRC cell proliferation.
- HDAC5 knockdown suppresses CRC cell growth.
- HDAC5 upregulates DLL4 expression, which mediates its proliferative effects.
Conclusions:
- HDAC5 promotes colorectal cancer cell proliferation via DLL4 upregulation.
- HDAC5 represents a potential therapeutic target for colorectal cancer treatment.
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