BMAP-27 Peptide Reduces Proliferation and Increases Apoptosis in Primary and Metastatic Colon Cancer Cell Lines

Abstract

BMAP-27 peptide is reported to possess apoptotic and anti-proliferative effects against cancer cells but the actual mechanism of action is yet to be investigated. In the current investigation, we aimed to study the role of the BMAP-27 peptide in reducing proliferation and increasing apoptosis in colon cancer cell lines. In this study, we used primary and metastatic colon cancer cell lines SW480 and SW620. Cell proliferation was measured using MTT and CCK-8 assays, and cellular damage was analyzed by lactate dehydrogenase assay. Apoptosis, cell cycle, and proliferation potentials were measured by the expression of CASPASE3, BAX, BCL-2, TP53, CDK-6, PCNA, WNT11, AXIN1, and CTNNB1 genes. Additionally, in-silico studies were conducted to determine the binding affinities of BMAP-27 with adenomatous polyposis coli (APC) and β-catenin proteins, one of the primary regulators of colon cancer. BMAP-27 peptide reduced colon cancer cell proliferation, upregulated tumor suppressor genes CASPASE3, BAX, TP53, AXIN1 expression, and downregulated the expression of oncogenes BCL-2, CDK-6, PCNA, WNT11, CTNNB1 in both the cell lines, however, in the primary colon cancer cell line the changes are found to be more significant. The molecular dynamic simulation analysis revealed substantial binding affinity of the peptide to APC and β-catenin proteins. BMAP-27 peptide significantly inhibited the proliferation and induced apoptosis in the primary colon cancer cell line than in the metastatic colon cancer cell line. In-silico results suggest that BMAP-27 shows a strong binding affinity with APC and β-catenin proteins, highlighting its role in inhibiting colon cancer cell proliferation.

Integrated Bioinformatics Analysis and Transcriptomics Analysis Predict Jumonji and AT Rich Interacting Domain2 (JARID2) as a Therapeutic Target in Human Cancers

“…Each type of cancer possesses a unique molecular signature, which could be any alterations in genetic and epigenetic events (Li et al, 2011;Randall et al, 2014;Takeshima and Ushijima, 2019;Ghosh et al, 2024;Yadav et al, 2024). Apart from genetic aberrations, epigenetic changes play an inevitable role in promoting malignancy (You and Jones, 2012;Das et al, 2024;Halder, 2024). The cancer cells proliferate and perform metastasis via a trigger regulated by certain driver genes, which stimulate tumor growth.…”