ArticleTranslational breast cancer research : a journal focusing on translational research in breast cancer2025
The impact and mechanisms of CRIP2 on the biological behavior of triple-negative breast cancer cells.
Article in Translational breast cancer research : a journal focusing on translational research in breast cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Triple-negative breast cancer (TNBC) is a distinct form of breast cancer that poses a significant threat to patients due to its high invasiveness, high recurrence and metastasis rates, and its lack of clear and definitive therapeutic targets. Cysteine-rich intestinal protein 2 (CRIP2, GeneID 1397) plays a role in many diseases, including cancer. However, its effect on proliferation and invasion of TNBC and its mechanism are not yet fully elucidated. The study aims to investigate the role and mechanism of CRIP2 (GeneID 1397) in the development and progression of TNBC and preliminary exploration of the relationship between CRIP2 and MAP2K4. Methods: Bioinformatics tools, GEPIA and UALCAN, were used to analyze CRIP2 expression in breast cancer tissues and normal breast tissues from The Cancer Genome Atlas (TCGA) database. Western blot (WB) was utilized to detect the expression differences of CRIP2 in normal breast epithelial cells and breast cancer cells. The effects of CRIP2 on breast cancer cell proliferation were examined using Cell Counting Kit-8 (CCK-8) and EdU assays. The impact of CRIP2 on breast cancer cell migration and invasion was assessed through Transwell assays. The influence of CRIP2 on NF-κB pathway marker proteins p65 and phosphorylated p65 was evaluated by WB. Potential interacting proteins of CRIP2 were predicted using the Biogrid database. Results: (I) UALCAN and GEPIA databases revealed that CRIP2 expression is higher in breast cancer tissues compared to normal breast tissues. (II) CCLE database cell expression profiles and WB showed that CRIP2 expression in TNBC cells is lower than in other breast cancer subtypes. (III) CCK-8, EdU, and Transwell assays confirmed that upregulating CRIP2 inhibits the proliferation, migration, and invasion capacities of MDA-MB-231 cells. (IV) WB indicated that upregulating CRIP2 can inhibit the expression of phosphorylated p65 protein. (V) Upregulation of CRIP2 can reverse the proliferation, migration, and invasion capacities of breast cancer cells overexpressing MAP2K4. Conclusions: Up-regulation of CRIP2 inhibits the proliferation, migration and invasive capacity of MDA-MB-231 cells, up-regulation of CRIP2 inhibits P65 phosphorylation, over-expression of MAP2K4 down-regulates CRIP2 expression, and up-regulation of CRIP2 reverses the ability of MAP2K4 over-expression to promote the malignant phenotype of breast cancer.
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