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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Cell Signal. 2022 Mar 12;94:110306. doi: 10.1016/j.cellsig.2022.110306

Fig. 1.

Fig. 1.

TRPM7 functions as a positive regulator of lncRNA HOTAIR. We used the TRPM7 KN2.0 human gene knockout via CRISPR, a non-homology mediated kit from OriGene to knockout all the splicing variants of the TRPM7 gene in A172 glioma cells. A, Two of A172 stable cell lines with TRPM7 deletion (A172 KO1 and A172 KO2) were generated after puromycin selection. TRPM7 knockout was confirmed by GFP positive cells (upper panel), reduced expression of TRPM7 mRNA by qPCR (middle panel), and reduced TRPM7 protein expression on Western blot (lower panel). B-D, A172 KO1 was the most efficient to be selected for further experiments and is labeled as A172 KO. Total RNA from glioma cells either with A172 or A172 KO cells were extracted and then subjected to Human Cancer Pathway Finder, RT2 lncRNA PCR Array. Data analysis from RT2 data resulted in a list of 10 downregulated and 7 upregulated lncRNAs whose transcripts are statistically significant with fold changes greater than 2.0 by TRPM7 knockout. B, A list of the IncRNAs with a fold change greater than 2.0. C, the scatter plot, and D, heat map.