Enhancement of resistance to chemo-radiation by hsa-miR-1290 expression in glioblastoma cells.

One of the resistance mechanisms to chemo-radiation is the efficiency of the DNA repair systems. MicroRNAs can alter the expression of their involved proteins; therefore, it may lead to a change in the response of cancer cells to adjuvant treatments. Here, the present study is aimed to investigate the role of hsa-miR-1290 on the chemo-radiation resistance and the target genes in the glioblastoma cells. First, we altered miR-1290 expression in the U-87 cells by using hsa-miR-1290 mimic and anti-miR-1290. Then, the Annexin V, CCK-8, MTT, colony formation, invasion, migration, and wound healing tests were utilized to study hsa-miR-1290 influences on cellular behavior such as proliferation, apoptosis, and metastasis. Moreover, the qRT-PCR and Western blot analyses were used to evaluate the effects of miR-1290 on the SOCS4 gene expression. Our results represented that the overexpression of miR-1290 could increase cell proliferation, migration, invasion, and resistance to chemo-radiation. The results showed miR-1290 directly targeted the 3՛UTR of the SOCS4 gene and suppressed its expression. Moreover, the suppression of hsa-miR-1290 led to an increase of apoptosis and cellular sensitivity to chemotherapy drugs and could also lead to decrease cell proliferation, migration, and invasion. Our findings proposed that miR-1290 can function as a novel oncomiR in glioblastoma cells by regulating its downstream genes such as SOCS4. Moreover, hsa-miR-1290 may be employed as a therapeutic target for clinical therapy of glioblastoma.