2022
DOI: 10.1016/j.neo.2022.100820
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Overexpression of the miR-17-92 cluster in colorectal adenoma organoids causes a carcinoma-like gene expression signature

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Cited by 7 publications
(2 citation statements)
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“…This amplification is associated with CRC progression and plays a crucial role in the transition from colorectal adenoma to carcinoma. It is also implicated in the promotion of 13q chromosomal gain [ 27 ]. Additionally, during the transition from colorectal adenoma to adenocarcinoma, there is a notable increase in miR-17-92 cluster expression, which is linked to DNA copy number gains at the miR17-92 locus on chromosome 13q31 and heightened c-Myc expression.…”
Section: Mechanisms Underlying Altered Mir-17-92 Expression In Colore...mentioning
confidence: 99%
“…This amplification is associated with CRC progression and plays a crucial role in the transition from colorectal adenoma to carcinoma. It is also implicated in the promotion of 13q chromosomal gain [ 27 ]. Additionally, during the transition from colorectal adenoma to adenocarcinoma, there is a notable increase in miR-17-92 cluster expression, which is linked to DNA copy number gains at the miR17-92 locus on chromosome 13q31 and heightened c-Myc expression.…”
Section: Mechanisms Underlying Altered Mir-17-92 Expression In Colore...mentioning
confidence: 99%
“…Downregulation of TS-miR- The miR-17-92 cluster (miRs-17, -18a, -19a, -20a, -19b, and -92a) downregulates PTEN (phosphate and tensin homolog), E2F, the transforming growth factor-β (TGF-β) signaling pathway, B cell lymphoma/leukemia 2-like protein 11 (BCL2L11), and thrombospondin-1 (TSP-1) [8]. Functionally, it favors tumor growth and is reported to be overexpressed in small-cell lung cancer, colon cancer, hepatocellular carcinoma, thyroid cancer, colorectal adenoma organoids, and renal cell carcinoma [9][10][11][12][13][14].…”
Section: Role Of Mirnas In Cancermentioning
confidence: 99%