Retracted: Anticancer effects of miR‐200c in colorectal cancer through BMI1

Abstract

Colorectal cancer (CRC) is one of the most leading cancer deaths throughout the world. MiR-200c has been shown to have a critical role in cancer initiation and progression. In this study, we investigated the miR-200c expression in CRC tissues and its effects on CRC cell lines which were mediated by polycomb complex protein (BMI1). Quantitative reverse transcription polymerase chain reaction (QRT-PCR) and immunohistochemistry were used to detect miR-200c and BMI1 expression in tumor tissues from 38 patients with CRC and 38 normal colon tissues. HCT-116 and SW-48 cells were transfected by locked nucleic acid (LNA)-anti-miR-200c. Western blot analysis and real-time PCR were applied to determine the BMI1 protein and microRNA (miRNA) levels. The apoptosis was analyzed via annexin/propidium iodide staining, and cell invasion was evaluated by transwell assay. MiR-200c was markedly downregulated in CRC tissues, whereas the protein expression of BMI1 in CRC tissues was upregulated compared with normal colon tissues. In the colon cancer cell lines, transfection of LNA-anti-miR-200c increased BMI1 gene and protein expression as well as the cell invasion. Downregulation of miR-200c by LNA decreased the apoptotic cells. The results from this study revealed that miR-200c may have antitumor effects through inhibition of BMI1 expression.

SEMA4D Knockdown Attenuates β-Catenin-Dependent Tumor Progression in Colorectal Cancer

“…CRC remains one of the leading cause of human malignancies worldwide [29]. Although pioneering treatment strate-gies have been made, its morbidity and mortality are still substantial.…”

Assessment of clinicopathological and prognostic relevance of BMI‐1 in patients with colorectal cancer: A meta‐analysis

“…The PcG group family of proteins is introduced as transcriptional repressors, and key regulators of cancer development and progression. BMI‐1 is a proto‐oncogene that belongs to this family and its expression is associated with CSC phenotype [35].…”

Epigenetic‐based therapy for colorectal cancer: Prospect and involved mechanisms

“…Trichostatin A Induction of G1 cell-cycle arrest and apoptosis of CRC by upregulation of JAK2/STAT3 inhibitor SOCS1,3 via acting as HDACi (Xiong et al, 2012) Vorinostat Enhancing of CRC cells sensitivity to 5-FU by upregulation of P53 and TS downregulation via acting as HDACi (Di Gennaro et al, 2009) Valproic acid Enhancing of CRC cells sensitivity to bosutinib by c-Src inhibition via acting as HDACi (Mologni et al, 2009) SIRT-1 Inhibition of CRC metastasis by AP-1 suppression via acting as HDACi (L. N. Sun et al, 2017) SIRT-6 Inhibition of CRC cells survival and proliferation by target CDC25A via acting as HDACi (W. Panobinostat Inhibit of CRC proliferation and colony formation by downregulation of EGFR, HER2, HER3, NF-κB1, IRAK1, and CCND1 via acting as HDACi (LaBonte et al, 2011) MS-275 Inhibition of CRC proliferation by activation of HDAC3, 4 via acting as HDACi (Lutz et al, 2016) EPZ-6438 Induction of CRC cell-cycle arrest in G1/S phase via acting as EZH2 inhibitor (J. F. Chen et al, 2016) UNC-1999 Induction of CRC apoptosis, ER stress, and UPR via acting as EZH2 inhibitor (Hsieh et al, 2016) 4SC-202 Inhibition of CRC proliferation and apoptosis induction by suppression of Akt expression via acting as HDACi (Zhijun et al, 2016) GSK343 Inhibition of CRC proliferation and metastasis via acting as EZH2 inhibitor (Ying et al, 2017) DZNep Inhibition of CRC proliferation and induction of cell-cycle arrest and apoptosis by upregulation of p27 and downregulation of p-CDC2 expression via acting as EZH2 inhibitor (Sha et al, 2015) 5-Azanucleosides Inhibition of CRC viability by suppression of the PI3K/Akt signaling pathway via acting as DNMT inhibitor (Pawlak et al, 2016) 5-AzaDC Inhibition of CRC growth by suppression of JAK2/STAT3/STAT5 signaling via acting as DNMT inhibitor (Xiong et al, 2009) CBB1003 Suppresses of CRC growth through downregulation of leucine-rich repeat-containing G-protein-coupled receptor 5 expression via acting as HDACi (Hsu et al, 2015) miR-34a Suppressing of CRC metastasis by targeting and regulating Notch signaling pathway via acting as tumor suppressor microRNA (X. miR-143 Inhibition of ERBB3 expression and CRC invasion but not proliferation by acting as tumor suppressor microRNA (Bai et al, 2016) miR-490-3p Suppressing of CRC metastasis through inhibition of TGF-β signaling by acting as tumor suppressor microRNA (X. Xu et al, 2015) miR-140 Suppressing of CRC metastasis by inhibition of EMT through acting as tumor suppressor microRNA miR-200c Suppressing of CRC metastasis by inhibition of BMI-1 expression through acting as tumor suppressor microRNA (Karimi Mazraehshah et al, 2018) miR-152 Suppressing of ...…”