Retracted: microRNA‐29b inhibits cell growth and promotes sensitivity to oxaliplatin in colon cancer by targeting FOLR1. (17th October 2019)

• Record Type: Journal Article
• Authors: Fu, Qiang; Zhang, Jindai; Huang, Gaofeng; Zhang, Yonglei; Zhao, Minghai; Zhang, Yongchao; Xie, Jianguo
• Is Part Of: BioFactors. Volume 46:Number 1(2020)
• Page Start: 136
• Page End: 145
• Publication Date: 2019-10-17
• Subjects: cell growth -- colon cancer -- folate receptor 1 -- microRNA‐29b -- oxaliplatin -- sensitivity; Vitamins -- Physiological effect -- Periodicals; Trace elements -- Physiological effect -- Periodicals; Growth factors -- Physiological effect -- Periodicals; Plant growth promoting substances -- Physiological effect -- Periodicals; Biochemistry -- Periodicals; Nutritional Physiological Phenomena -- Periodicals; Trace Elements -- metabolism -- Periodicals; Vitamins -- metabolism -- Periodicals; Molecular Biology -- Periodicals; 612.399
• DOI: 10.1002/biof.1579
• Languages: English
• ISSNs: 0951-6433

Abstract

Abstract: The present study was aimed to explore the functional role of microRNA (miR)‐29b in colon cancer, as well as underlying mechanisms. Expressions of miR‐29b and folate receptor 1 (FOLR1) were measured in both human colon tumor samples and cell lines. Colon cancer cell lines SW480 and SW620 were transfected with miR‐29b mimic, antisense oligonucleotides (ASO)‐miR‐29b, small interfering (siRNA) against FOLR1 (si‐FOLR1), or corresponding negative controls (NCs), and then were incubated with or without oxaliplatin (L‐OHP). Thereafter, cell viability, cytotoxicity, cell apoptosis, and expression of FOLR1, ATP Binding Cassette Subfamily G Member 2 (ABCG2) and p‐glycoprotein (p‐gp) were analyzed. We found that miR‐29b was significantly decreased, while FOLR1 was statistically elevated in colon cancer samples and cell lines compared to the nontumor samples and nontumourigenic immortalized human colon epithelial cell line FHC. Overexpression of miR‐29b markedly inhibited cell viability, promoted sensitivity to L‐OHP, stimulated cell apoptosis (all p < .05), and decreased the levels of ABCG2 and p‐gp in cancer cells, whereas suppression of miR‐29b showed contrary results. Moreover, we observed that FOLR1 was a direct target of miR‐29b and was negatively regulated by miR‐29b. In addition, the findings revealed that the effects of FOLR1 inhibition on cell viability, sensitivity to L‐OHP, cell apoptosis, and the levels of ABCG2 and p‐gp were similar to overexpression of miR‐29b. Taken together, our study suggests that miR‐29b inhibits cell growth and promotes sensitivity to L‐OHP in colon cancer by targeting FOLR1. Highlights: miR‐29b is decreased, while FOLR1 is elevated in cancer samples and cell lines; miR‐29b inhibits cell growth and promotes sensitivity to L‐OHP in cancer cells; FOLR1 is a direct target of miR‐29b; FOLR1 promotes cell growth and inhibits sensitivity and apoptosis in cancer cells; Effects of miR‐29b on cell growth and sensitivity might be by targeting FOLR1.