| Summary: | Bustanur Rosidi,1 Diana Priyatno,1 Teguh Pribadi Putra,1 Irawan Yusuf1,2 1Division of Proteomics, Mochtar Riady Institute for Nanotechnology and Medical Science Group, University of Pelita Harapan, Tangerang, Banten, Indonesia; 2Faculty of Medicine, Hasanuddin University, Makassar, IndonesiaCorrespondence: Bustanur Rosidi; Irawan Yusuf, Mochtar Riady Institute for Nanotechnology and Medical Science Group, University of Pelita Harapan, Jalan Boulevard Jenderal Sudirman 1688, Lippo Karawaci, Tangerang, Banten, 15811, Indonesia, Tel +62 21-54210123, Email brosidi@mrinstitute.org; irawanyusufgenome@gmail.comPurpose: To study the effects of metformin on the proliferation and growth of human colorectal cancer cell lines HCT116 and SW620.Materials and Methods: The antiproliferative effect of metformin was assayed using an MTS reagent and its ability to inhibit colony formation was demonstrated using a clonogenic assay. Flow cytometry using YO-PRO-1/PI was performed to examine the effects of metformin on apoptosis and cell death of HCT116 and SW620. Caspase 3 activities were measured in caspase-3 activity tests using a caspase-3 activity kit. Furthermore, Western blots were performed with anti-PARP1, anti-caspase 3, and anti-cleaved caspase 3 to confirm whether caspase activation was present or not.Results: Both MTS proliferation assays and clonogenic assays showed that metformin inhibited the proliferation and growth of HCT116 and SW620 cells in a concentration-dependent manner. Flow cytometric analysis identified early apoptosis and metformin-induced cell death in both cell lines. However, caspase 3 activity could not be detected. Cleavage of both PARP1 and pro-caspase 3 was not observed in the Western blot, confirming the absence of caspase 3 activations.Conclusion: This present study suggests a caspase 3-unrelated apoptosis mechanism of metformin-induced cell death in human colorectal cancer cell lines HCT116 and SW620.Keywords: metformin, colorectal cancer, PARP1, anti-proliferative, apoptosis
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