【Animal Modeling】-The effect of long non-coding RNALINC00152 on the growth of human glioma xenografts in nude mice and its mechanism

  The effect of U251 tumor-bearing mice on tumor growth and its mechanism were discussed.

  Methods: LINC00152 expression level of U251 cells was up-regulated by lentivirus transfection, LINC00152 overexpression group (LV-LINC00152 group) and empty control group (LV group) were established, and normal U251 cells were used as blank control group (control group); qRT -PCR was used to detect the expression level of LINC00152; U251 tumor-bearing mouse model was constructed, treated with p-YAP inhibitor XMU-MP-1, the tumor volume was measured, and the end point of the experiment was weighed; the expression of Ki67 in tumor tissue was observed by immunohistochemical staining; Western blotting The protein expression of YAP, p-YAP, LATS1 and pLATS1 was detected experimentally.

  Results: Compared with the LV group, the expression of LINC00152 in the LV-LINC00152 group was significantly up-regulated (P<0.01). At the end of the experiment, compared with the tumor-bearing mice of the LV group, the tumor volume of the LV-LINC00152 group was significantly increased, and the tumor weight was significantly increased (P<0.01); XMU-MP-1 (1mg/kg and 3mg/kg) treatment significantly reduced the tumor volume and tumor weight of the LV-LINC00152 group of tumor-bearing mice (P<0.01) in a dose-dependent manner. Tumors in the LV group The tissue Ki67 showed weakly positive expression, while the LV-LINC00152 group showed strong positive expression; after XMU-MP-1 (1 mg/kg and 3 mg/kg) treatment, the two tumor tissues showed weak and positive Ki67 expression. Compared with the LV group, the The expression of p-YAP and p-LATS1 protein in tumor tissue of LV-LINC00152 group was significantly up-regulated (P<0.01); XMU-MP-1 (1mg/kg and 3mg/kg) treatment could reverse the expression of p-YAP and p-LATS1 protein (P<0.01). P < 0.01), and there was a dose-dependent manner.

  Conclusion: Long non-coding RNALINC00152 can induce YAP phosphorylation and promote the growth of glioma, and the p-YAP inhibitor XMU-MP-1 can inhibit the above biological effects of long non-coding RNALINC00152.