Primary Colon Cancer Cell Lines Research Articles

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

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.

Exosomes from metastatic colon cancer cells drive the proliferation and migration of primary colon cancer through increased expression of cancer stem cell markers CD133 and DCLK1

The exchange of biological material between the neighbouring cells is essential for homeostasis. In pathological conditions, such as cancer, the major challenge in cancer treatment is the abnormal expression of crucial proteins and miRNA exchanged between the cancer cells through extracellular vesicles called exosomes. Clinically, it has been noticed that the primary tumour and the distal metastases are interconnected and co-dependent. The exosomes are key factors responsible for preparing the pre-metastatic niche and communicating between the tumour and the distal metastatic site. Cancer stem cells (CSCs) are a subpopulation of cancer cells with self-renewal characteristics and are shown to be responsible for metastasis. This study aims to understand the effect of metastatic cell line-derived exosomes and their regulation of CSC marker expressions on primary colon cancer cell lines. We have identified that treatment of primary colon cancer cell lines with metastatic colon cancer cell-derived exosomes has significantly increased the proliferation, colony formation, cell migration, and invasion. In addition, there was a significant increase in the number and size of spheroids following the exosomes treatment. We found that this metastatic phenotype is due to the increased expression of CD133 and DCLK1 in primary colon cancer cells.

Effect of extremely low frequency electromagnetic fields on a-Lactalbumin and Sulindac treated colon cancer cells: ELF-EMF and colon cancer

Aim: In this research, we aimed to investigate the effects extremely low frequency electromagnetic fields (ELF-EMF) on proliferation and apoptosis during treatment of primary and metastatic colon cancer cell lines. Material and Methods: Colon cell lines; COLO-320, COLO-741 and as control mouse fibroblast (STO) cells were cultured in 24 wells of tissue culture plate. Both COLO-320 and COLO-741 cells were treated with α-lactalbumin, sulindac and α-lactalbumin + sulindac. The cells from all groups were exposed to 60 Hz ELF-EMF for 48 hours. For cytotoxicity analyses, the cells were collected and analyzed with ELISA. The cells were fixed in 4% paraformaldehyde for 30 minutes. Cell proliferation was analyzed by evaluating of anti-Ki-67 distribution using indirect immunohistochemistry, cell death were evaluated using TUNEL assay. Results: After TUNEL assay, the TUNEL positive cells were detected in all treated and control groups. However, the number of apoptotic cells was increased after treatment with α-lactalbumin and EMF exposure on COLO-320 cells. The apoptotic cells were less in STO cells. The distribution of Ki-67 was also detected in all groups, but, there were more Ki-67 immunoreactivity in COLO-741 cells than other groups. The cell cytotoxicity was also increased after EMF exposure in all groups. Discussion: Our results suggested that the EMF exposure may increase the effects of α-lactalbumin on primary colon cancer cell lines. However, the proliferation of both cancer and control cells were not affected. The EMF exposure may trigger apoptotic pathway in primary colon cancer cell lines.