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DAC can restore expression of NALP1 to suppress tumor growth in colon cancer
11] Department of Clinical Biochemistry, Dalian Medical University, Dalian 116044, China [2] Department of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, China.
Abstract:
Despite recent progress in the identification of genetic and molecular alternations in colorectal carcinoma, the precise molecular pathogenesis remains unclear. NALP1 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 1) is a member of the nucleotide-binding oligomerization domain-like receptor family of proteins that are key organization proteins in the inflammasome. It is reported that NALP1 plays a central role in cell apoptosis, pyroptosis, inflammatory reactions and autoimmune diseases. DAC (5-aza-2-deoxycytidine) is an antitumor drug useful to lung cancer, myelodysplastic disorders, myelodysplasia and acute myeloid leukemia. In this study, we examined the expression of NALP1 in human normal and cancerous colon tissues using tissue microarray, western blot and quantitative real-time PCR and we measured the expression of NALP1 in three kinds of colon cancer cell lines and animal models before and after treatment with DAC. Furthermore, we examined the treatment effects of DAC on colon cancer in our animal model. Our data indicate that NALP1 is expressed low in human colorectal tumoral tissues relative to paratumoral tissues and was associated with the survival and tumor metastasis of patients. The expression of NALP1 increased after treatment with DAC both in vitro and in vivo. Furthermore, DAC suppressed the growth of colon cancer and increased lifespan in mouse model. Therefore, we conclude that NALP1 is expressed low in colon cancer and associated with the survival and tumor metastasis of patients, and treatment with DAC can restore NALP1 levels to suppress the growth of colon cancer.
Insights
NALP1 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 1) is underexpressed in colorectal cancer, correlating with poor patient survival. The antitumor drug DAC (5-aza-2-deoxycytidine) effectively restores NALP1 levels and suppresses tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Colorectal carcinoma pathogenesis remains incompletely understood despite advances in genetic and molecular alterations.
- NALP1, a key inflammasome protein, is implicated in apoptosis, pyroptosis, inflammation, and autoimmune diseases.
- The antitumor drug 5-aza-2-deoxycytidine (DAC) is effective against various cancers.
Purpose of the Study:
- To investigate NALP1 expression in colorectal cancer tissues and cell lines.
- To determine the association of NALP1 expression with patient survival and tumor metastasis.
- To evaluate the effect of DAC on NALP1 expression and colon cancer growth in vitro and in vivo.
Main Methods:
- Tissue microarray, western blot, and quantitative real-time PCR were used to assess NALP1 expression in human colon tissues.
- NALP1 expression was measured in colon cancer cell lines and animal models before and after DAC treatment.
- Colon cancer treatment effects of DAC were examined in a mouse model.
Main Results:
- NALP1 expression was significantly lower in human colorectal tumoral tissues compared to paratumoral tissues.
- Low NALP1 expression was associated with reduced patient survival and increased tumor metastasis.
- DAC treatment increased NALP1 expression both in vitro and in vivo.
- DAC suppressed colon cancer growth and extended lifespan in a mouse model.
Conclusions:
- NALP1 is downregulated in colon cancer and linked to poorer survival and metastasis.
- DAC treatment can restore NALP1 levels, thereby inhibiting colon cancer progression.
- NALP1 may serve as a potential therapeutic target or biomarker in colorectal cancer.
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