By array analysis, there were 17 significantly down-regulated and 7 significantly up-regulated miRNAs in subjects who later developed neoplasia. miR-215 was significantly up-regulated both 1-2 years prior to the onset of neoplasia (3.5-fold, <i>p</i> < 0.001) and 3-5 years prior to the onset of neoplasia (5.4-fold, <i>p</i> = 0.007). miR-215 expression was also increased in UC-associated colon cancers (5.3-fold, <i>p</i> = 0.03) and adjacent non-dysplastic UC tissue (6.2-fold, <i>p</i> = 0.02). p53 was expressed in 20% of patients prior to the onset of neoplasia and in 67% of UC-associated colon cancers, although was not correlated with miR-215 expression.
The effects of miR-215-3p on colon cancer cell growth and apoptosis were investigated using cell counting kit-8 (CCK-8) and apoptosis assay, respectively.
There are accumulating reports that microRNAs are dysregulated in a number of human cancer types, and that they may function as tumor suppressors or oncogenes in tumorigenesis and tumor development. microRNA-215 (miR-215) has been identified as a tumor suppressor in epithelial ovarian, pancreatic, non-small cell lung and colon cancer, whereas it may act as an oncogene in gastric and cervical cancer.
In vitro analyses showed that ectopic expression of miR-215 decreases viability and migration, increases apoptosis and promotes cell cycle arrest in DLD-1 and HCT-116 colon cancer cell lines.
Endogenous miR-215 was elevated about 3-fold in CD133+HI/CD44+HI colon cancer stem cells that exhibit slow proliferating rate and chemoresistance compared to control bulk CD133+/CD44+ colon cancer cells.