Colorectal cancer (CRC) is the most frequently diagnosed cancer and the most common gastrointestinal cancer worldwide. Due to the presence of populations of cancer stem cells (CSCs) that cause recurrence,… Click to show full abstract
Colorectal cancer (CRC) is the most frequently diagnosed cancer and the most common gastrointestinal cancer worldwide. Due to the presence of populations of cancer stem cells (CSCs) that cause recurrence, the possibility of cancer treatment is very low. The aim of current study was to evaluate the inhibitory role of miR‐200c on EMT, CSCs markers and β‐catenin in HCT‐116 and SW48 cell lines. The expression of miR‐200c, EMT‐related genes, CSCs markers, and β‐catenin were quantified by qRT‐PCR. Further, expression of β‐catenin and EMT‐related proteins, and migration were analyzed by Western blot, and migration assay kit, respectively. Spheroid formation assay was used to enrich colorectal CSCs from colorectal cancer cell lines. LNA‐anti‐miR‐200c suppressed the endogenous miR‐200c in transfected cells compared with the control. qRT PCR and Western blot analysis of LNA‐anti‐miR‐200c transfected cells revealed a considerable increase in CSCs markers, vimentin, ZEB‐1, N‐cadherin, and β‐catenin expression, with a concomitant reduction in E‐cadherin expression level. Migration and sphere forming ability of HCT‐116 and SW48 cells increased in transfected cells. The results of current study revealed that downregulation of miR‐200c may be an important factor for the overexpression of CSCs markers and EMT related genes via β‐catenin upregulation in CRC.
               
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