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Study on SNHG17 regulates the malignant phenotype of glioblastoma by regulating miR-23b-3p and ZHX1 |
GE Beihai1 ZHOU Wei2 WEI Ninglin1 ZHANG Xian1 MO Yun1 SU Zhou1 QIN Guangping1 XU Guolong1 |
1.Department of Neurology, Guangxi Zhuang Autonomous Region Brain Hospital, Guangxi Zhuang Autonomous Region, Liuzhou 545005, China; 2.Department of Neurosurgery, Guangxi Zhuang Autonomous Region Brain Hospital, Guangxi Zhuang Autonomous Region, Liuzhou 545005, China
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Abstract Objective To detect detection of small nucleolar RNA host gene 17 (SNHG17) How to regulate malignant phenotype of glioblastoma (GBM) by miR-23b-3p and zinc finger structure homeobox protein 1 (ZHX1). Methods Surgical specimens of 33 patients diagnosed with GBM in the Department of Neurosurgery, the Guangxi Zhuang Autonomous Region Brain Hospital from January 2020 to October 2022 were selected. The expression of SNHG17, miR-23b-3p, and ZHX1 in GBM samples and normal tissues adjacent to tumor were detected by real-time quantitative polymerase chain reaction (qRT-PCR). Pearson correlation analysis was used to evaluate the correlation between SNHG17, miR-23b-3p, and ZHX1. GBM cell line A172 and DK-MG were used as cell models, the cells were divided into si-NC group (transfected with blank inhibitor), si-SNHG17 group (transfected with si-SNHG17#2), and si-SNHG17+miR-23b-3p inhibitor group (transfected with si-SNHG17#2 and miR-23b-3p inhibitor). The proliferation capacity of GBM cells was detected by CCK-8 and EdU methods, while the migration and invasion of GBM cells were evaluated by Transwell assay. The qRT-PCR and Western blot were used to detect the mutual regulation of SNHG17 and miR-23b-3p, and their regulatory effect on ZHX1. Results The expression levels of SNHG17 and ZHX1 in GBM tissue were higher than those in normal tissue adjacent to cancer, while the expression level of miR-23b-3p was lower than that in normal tissue adjacent to cancer, the differences were statistically significant (P<0.05). In GBM tissues, SNHG17 expression was negatively correlated with the expression of miR-23b-3p (r=-0.711, P<0.05), but positively correlated with the expression of ZHX1 (r=0.648, P<0.05); the expression of miR-23b-3p and ZHX1 was negatively correlated (r=-0.637, P<0.05). The expression of miR-23b-3p in the si-SNHG17 group was higher than that in the si-NC group, and the proliferation, migration, and invasion ability of GBM cells and the expression level of ZHX1 were lower than those in the si-NC group, the differences were statistically significant (P<0.05); however, the expression of miR-23b-3p in the si-SNHG17 + miR-23b-3p inhibitor group was lower than that in the si-SNHG17 group, and the proliferation, migration, invasion, and expression level of ZHX1 in GBM cells were higher than those in the si-SNHG17 group, the differences were statistically significant (P<0.05). Conclusion SNHG17 can promote the proliferation, migration and invasion of GBM cells by regulating miR-23b-3p/ZHX1 axis. This suggests that SNHG17 may be a potential therapeutic target for GBM.
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