ArticleMedical journal, Armed Forces India
The effects of miR-217 inhibitor and mimic in the progression of Kirsten rat sarcoma viral oncogene homologue driven cancers.
Article in Medical journal, Armed Forces India. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- miR-4326 predicts adverse outcomes of triple-negative breast cancer and regulates cell growth and motility through modulating MED13.World journal of surgical oncology · 2026Article
- Genomic insights into Marinospirillum alkalitolerans sp. nov., a novel PHB producing bacterium from an Indian impact crater, and an emended description of family Oceanospirillaceae.Antonie van Leeuwenhoek · 2025Article
- Lab sciences: Going beyond the realms of diagnosis!!Medical journal, Armed Forces IndiaArticle
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8 authors.
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Abstract
Background: 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 Method: 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 Results: 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. Conclusion: 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.
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