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Heterozygous loss of Dip2B enhances tumor growth and metastasis by altering immune microenvironment
Salah Adlat1, Farooq Hayel2, Yang Chen3
1Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510100, China; Transgenic Research Center, School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, China.
Abstract:
Cancer is caused by abnormal cell growth and metastasis to other tissues. Development of cancers is complex and underlining mechanisms are mostly unknown. Disco-interacting protein 2 homolog B (DIP2B) is a member of Dip2. There have been reports suggesting that Dip2B may participate in tumor growth and development. However, direct link between DIP2B and cancer development is missing. In this study, Dip2btm1a/+ heterozygous knockout mouse model was used to investigate tumor growth and metastasis. Results show that one allele knockout of Dip2B significantly promoted tumor growth and metastasis, decreased tumor cell apoptosis and reduced immune cell infiltration in tumors, most likely by altering immune system that includes reduction of macrophage and cytotoxic T-cells infiltration into tumor microenvironment.
Insights
Disco-interacting protein 2 homolog B (DIP2B) deficiency promotes cancer growth and metastasis. Reduced DIP2B function impairs anti-tumor immunity by decreasing immune cell infiltration, including macrophages and cytotoxic T-cells.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Cancer arises from uncontrolled cell growth and spread.
- The precise mechanisms driving cancer development remain largely unknown.
- Disco-interacting protein 2 homolog B (DIP2B) is implicated in tumor progression, but its direct role is unclear.
Purpose of the Study:
- To investigate the role of DIP2B in tumor growth and metastasis.
- To elucidate the impact of DIP2B on the tumor microenvironment and immune response.
Main Methods:
- Utilized a heterozygous knockout mouse model (Dip2btm1a/+) to study DIP2B function.
- Analyzed tumor growth, metastasis, apoptosis, and immune cell infiltration.
Main Results:
- Heterozygous knockout of DIP2B significantly enhanced tumor growth and metastasis.
- Reduced DIP2B levels decreased tumor cell apoptosis.
- Observed diminished infiltration of immune cells, including macrophages and cytotoxic T-cells, into the tumor microenvironment.
Conclusions:
- DIP2B plays a crucial role in suppressing cancer progression.
- Altering DIP2B levels impacts the anti-tumor immune response.
- DIP2B deficiency promotes a pro-tumorigenic environment by modulating immune cell infiltration.
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