Ethacridine Regulation of JAK/STAT/ERK Signaling Pathway in Colon Cancer Cells SW620: In vitro Approach

Abstract

Background Ethacridine have anticancer effects by inhibiting regulatory transcription factors and cell viability in various cancer cells. To investigate the effect of ethacridine on colorectal cancer cell lines, SW620 was studied via regulation of JAK/STAT/ERK signaling pathway. Materials and Methods Different doses of ethacridine (5–35 µM) expressed antiproliferative effects by decreasing the viability in a dose-dependent manner and the IC50 value was found to be 10 µM. Results Subsequent treatment with 10 µM of ethacridine showed that it induced mitochondrial dysfunction and reactive oxygen species generation. DAPI and PI staining assays revealed prominent apoptotic cells under the microscope when treated with 10 µM of ethacridine. In the mRNA expression study performing RT-PCR of apoptotic markers, cyclin-D1, Bax, Bcl-2, caspase 3, C-Myc, and surviving, enhanced levels of these markers were suppressed, which was inversely proportional to the levels of apoptotic enhancers namely Bax and caspase-3. It was also observed that increased NF-κB, IL-6, TNF-α, and COX-2 in colorectal cancer are suppressed by ethacridine. The expressions of JAK/STAT/ERK were also significantly suppressed after ethacridine treatment in SW620 cell lines. Conclusion In summary, it was corroborated that ethacridine promoted apoptosis in colon cancer cells by inhibiting quite a few cell signaling factors.