Knockout of Long Noncoding RNA SNHG16 Gene by CRISPR/Cas9 System Enhanced Expression of CD235a in K562 Cells
Guo Qing, Xu Changlu, Ma Yige, Wang Bingrui, Zhao Yanhong, Wang Ding, Zhang Yingnan, Huang Xin, Liu Jinhua, Gao Jie*, Shi Lihong*
The aim of this work was to investigate the effect of long noncoding RNA SNHG16 knock-out on human chronic myeloid leukemia cells (K562 cells). The SNHG16 gene in K562 cells was knocked out by using CRISPR/Cas9 system. Single cells were gained by flow cytometric sorting technique. SNHG16+/– and SNHG16–/– cell lines were gained after culture, identification of PCR and sequencing. The effects of SNHG16 depletion on morphology, proliferation, cell surface marker and erythroid transcription factors of K562 cells were detected by Wright-Giemsa staining, MTS assay, flow cytometry, and qRT-PCR. The results indicated that SNHG16 depletion did not affect the morphology and proliferation of K562 cells, but promoted the expression level of K562 cell surface marker CD235a and erythroid transcription factors. In conclusion, long noncoding RNA SNHG16 does not affect the proliferation of K562 cells, but SNHG16 plays a role in the regulation of K562 cell surface marker protein CD235a.
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