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Retracted : Anticancer effects of miR‐200c in colorectal cancer through BMI1
Author(s) -
Karimi Mazraehshah Mitra,
Tavangar Seyed Mohammad,
Saidijam Massoud,
Amini Razieh,
Bahreini Fatemeh,
Karimi Dermani Fatemeh,
Najafi Rezvan
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27330
Subject(s) - bmi1 , propidium iodide , colorectal cancer , cancer research , western blot , downregulation and upregulation , microrna , transfection , apoptosis , microbiology and biotechnology , biology , cancer , cell culture , chemistry , programmed cell death , gene , biochemistry , genetics
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.