ArticleWorld journal of gastrointestinal oncology2023
MicroRNA-363-3p inhibits colorectal cancer progression by targeting interferon-induced transmembrane protein 1.
Article in World journal of gastrointestinal oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mutations in untranslated non-coding regions of EGFR, AKT1 & HRAS modulate their expression regulatory networks to facilitate progression of colorectal cancer.Functional & integrative genomics · 2026Article
- The prognostic value of miR-363-5p in colorectal cancer and its associated molecular mechanisms.Hereditas · 2026Article
- A novel lipid droplet-related prognostic signature reveals CIDEC as a key biomarker for pancreatic adenocarcinoma.Frontiers in oncology · 2026Article
- Palmatine inhibits colorectal cancer proliferation and metastasis by regulating miR-363-3p/AURKA axis.Human cell · 2025Article
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Authors and funding
4 authors.
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Abstract
backgroundThe molecular mechanisms of colorectal cancer development and progression are far from being elucidated.
aimTo investigate the role of microRNA-363-3p (miR-363-3p) in the progression of colorectal cancer.
methodsReal-time polymerase chain reaction was performed to detect miRNA expression in human colorectal cancer tissues and paired normal colorectal tissues. PITA 6 was utilized to predict the targets of miR-363-3p. Dual-luciferase reporter system was used to validate the target of miR-363-3p. Plate colony formation assay and wound-healing assay were performed to evaluate cancer cells' clonogenic survival ability and migration ability, respectively. Cell proliferation was examined by cell counting kit-8 assay. Immunohistochemical staining was used to determine the expression level of interferon-induced transmembrane protein 1 (IFITM1) in colorectal cancer tissues and adjacent tissues. The TCGA and GTEx databases were used to compare the expression levels of
resultsMiR-363-3p was decreased in colorectal cancer tissues compared to normal colorectal tissues. IFITM1 was characterized as a direct target of miR-363-3p. Overexpression of miR-363-3p led to decreased clonogenic survival, proliferation, and migration of colorectal cancer cells, which could be reversed by forced IFITM1 expression.
conclusionMiR-363-3p can constrain clonogenic survival, proliferation, and migration of colorectal cancer cells
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