Aim
It is known that miR-504 can target p53 to promote cancer progression. Our bioinformatics analysis revealed that miR-504 could bind miR-143 host gene (miR143HG), suggesting that miR143HG might also have crosstalk with p53 in cancer progression. This study aimed to analyze the function of miR143HG in glioblastoma (GBM).
Conclusion
Therefore, miR143HG may decrease the proliferation of GBM cells by sponging miR-504 to upregulate p53.
Methods
This study selected 64 GBM patients. GBM and non-tumor tissues were obtained from the patients. RT-qPCR was used to analyze gene expression. Survival curve analysis was performed to analyze the prognostic values of miR143HG for GBM. The crosstalk between miR143HG and miR-504 was analyzed by overexpressing them in GBM cells, followed by RT-qPCRs to detect their expression. CCK-8 assay was used to detect the cell proliferation ability.
Results
We found that miR143HG was downregulated in GBM and predicted poor survival. The mRNA expression levels of miR143HG and p53 were positively correlated in GBM tissues. Bioinformatics analysis suggested that miR143HG could form base paring with miR-504, which has been reported to target p53. Overexpression experiments revealed that miR143HG overexpression upregulated the expression of p53, while miR-504 overexpression inhibited the effect of miR143HG overexpression on the expression of p53. Moreover, overexpression of miR143HG and p53 decreased GBM cell proliferation, while overexpression of miR-504 increased GBM cell proliferation. In addition, overexpression of miR-504 attenuated the effect of miR143HG overexpression on GBM cell proliferation.