| Autor: |
Misra, Pratibha, R, Palaniswamy, Boruah, Dibyajyoti, Gambhirrao, Ankita, Godse, Ruchira, Mk, Sibin, Gupta, Anurodh, Vashum, Yaongamphi |
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| Zdroj: |
Medical Journal Armed Forces India; Nov2024, Vol. 80 Issue 6, p702-711, 10p |
| Abstrakt: |
Kirsten rat sarcoma viral oncogene homologue (KRAS) is one of the most frequently mutated proto-oncogenes in approximately 90% of pancreatic ductal carcinoma (PDAC) and 45% of colorectal cancer (CC) cases. Studies in the past have identified microRNA-217 (miR-217) as a potential tumour-suppressing miRNA that is downregulated in various cancers. Using in silico prediction algorithms, several studies have identified miR-217 as a potential regulator of KRAS, and we investigated its role in PDAC and CC progression. The study was carried out in KRAS-driven cancer (KDC) cell lines PANC-1 (pancreatic cancer) and SW-480 (CC), which have mutant KRAS gene expression. The KDC cells are transfected with specific oligonucleotides for miR-217, anti-miR-217, and a negative control in serum-free media using lipofectamine. After fixing the IC 50 , using specific primers, gene expression studies were carried out by qPCR for KRAS downstream targets and genes associated with apoptosis and cell cycle. Anti-migration and anti-apoptotic effects were studied using the transwell migration assay and annexin-V/PI staining methods, and mitochondrial morphology was observed using a transmission electron microscope. The present study demonstrates that overexpression of miR-217 in KDC cells mitigates proliferation and migration and promotes cell cycle arrest and apoptosis of KDC cells via the MAPK/ERK signalling pathway. Besides, decreased miR-217 expression rescues KDC cells from the effects mediated by KRAS downstream signalling. The outcome of the study indicates miR-217 suppresses tumour growth and promotes apoptosis in KDC and that these effects are associated with down regulation of MAPK/ERK signalling. [ABSTRACT FROM AUTHOR] |
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