Discussion
We found that the loss of miR-210 altered a variety of cellular phenotypes including proliferation and apoptosis. Subsequent global gene expression analyses identified plausible mechanisms underlying these phenotypic changes in 293T cells. In particular, we showed that miR-210 might target the expression of BNIP3L as a potential mechanism to suppress apoptosis. Surprisingly, the mRNA levels of most previously reported miR-210 target genes were not induced upon miR-210 KO, suggesting a need to reexamining and studying human miR-210 functions directly and comprehensively. Thus, our work established a human cellular system and opportunity to unravel the complexity of the regulatory networks by miR-210.
Methods
To better investigate the functions and mechanisms of human miR-210, therefore, we derived the human miR-210 gene knockout (KO) 293T cell lines using the CRISPR/Cas9 technology. We then examined the cellular phenotypes and gene expression profiles of 293T cells under normoxia and hypoxia conditions.
