ZNF300 enhances temozolomide resistance in gliomas by regulating lncRNA SNHG12

Gliomas are the most common type of primary brain tumors, with high recurrence rate and mortality. In contrast to the high incidence, the prognosis of gliomas is dismal, and the therapeutic effect of temozolomide (TMZ), first-line chemotherapy drug for gliomas, is extremely limited by TMZ-resistance. ZNF300 is a member of zinc finger proteins, and promotes cell proliferation in several types of cancer. This study is designed to appraise the effects of ZNF300 on TMZ-resistance in gliomas. The TMZ-resistant glioma cell lines were established in U251 and A-172 cells. ZNF300 was significantly upregulated in TMZ-resistant glioma cells. ZNF300 depletion remodel TMZ sensitivity of glioma cells through inhibiting cell proliferation and promoting cell apoptosis. Meanwhile, ZNF300 depletion brought down-regulation of c-myc and SNHG12 which could be counteracted by overexpression of c-myc. Moreover, SNHG12 performed as the downstream of ZNF300 and c-myc, and overexpression of SNHG12 also could neutralize the effects of ZNF300 depletion on cell proliferation and cell apoptosis. Our data manifested that ZNF300 serves as a novel therapeutic target and biomarker of TMZ-resistant gliomas via mediating c-myc/SNHG12 pathway.