To Explore The Effect Of LncRNA SChLAP1 On Glioblastoma Proliferation And Invasion By The NF-κB Signaling Pathway

Background Glioblastoma(GBM)is the most common primary malignant brain tumor,and it is also the most aggressive malignant glioma,with a high recurrence rate.At present,the treatment of GBM is still not significantly effective.Great progress has been made in studying the role of long noncoding RNA(Lnc RNA)in the pathogenesis of glioma.Some scholars found that LncRNA SChLAP1 plays an important role in the proliferation and invasion of GBM,revealing the pathological processes of many diseases,including cancer initiation and progression;and NF-κB pathway was also found to play a key role in regulating GBM cell survival and proliferation.This study provides new ideas for the targeted therapy of glioblastoma by addressing the regulatory role and mechanism of target LncRNA SChLAP1 in the biological function of GBM cells.Objective To investigate the effects of LncRNA SChLAP1 on the proliferation and invasiveness of GBM.Methods(1)Collect samples of 25 patients with glioblastoma treated with surgery in the Neurosurgery Department of the People’s Hospital of the Affiliated Center of Three Gorges University from September 2020 to Three Gorges University from September 2020 to December 2022 for primary culture,The LncRNA SChLAP1 expression level in glioblastoma patient tissue and non-tumor brain tissue was determined by RT-PCR;(2)Using the Lnc RNASCh LAP1 expression level as the screening criterion,The highest expression in the primary cultured GBM cell lines,Using the lentivirus as a vector,Downregulate the LncRNA SChLAP1 expression level in tumor cells by transfection,The transfection efficiency was determined by RT-PCR;And(3)by dividing the GBM cells into five groups,Namely,the control,sh-SCh LAP1,sh-control,control-vector,and SCh LAP1-vector groups,The LncRNA SChLAP1 expression in each group was determined by PT-PCR,Transwell Analysis of the effect of LncRNA SChLAP1 on glioblastoma invasion ability;(4)The changes of cell activity and cell apoptosis ratio were detected by CCK-8 experiment and flow cytometry.(5)The changes of the NF-κB signaling pathway in the two groups were detected by western blot.Changes in protein HNRNPL associated to NF-κB signaling were detected after addition of inhibitors of NF-κB signaling pathway.Results(1)The Lnc RNASCh LAP1 expression level of GBM patients was significantly higher than non-tumor brain tissue(t=16.85,P<0.001);(2)The LncRNA SChLAP1 expression level in SCh LAP1-vector group was significantly higher than that in control-vector group,sh-control group and sh-SCh LAP1 group;(3)The RT-PCR results showed that the LncRNA SChLAP1 expression level of the SCh LAP1-vector group was higher than that of the negative control group(t=45.63,P<0.001),The LncRNA SChLAP1 expression level of the sh-SCh LAP1 group was lower than that of the negative control group(t=67.23,P<0.001).Transwell The experimental results showed that the number of penetrating cells in the field of the SCh LAP1-vector group(246 ± 10)was significantly higher than that in the control-vector group(127 ± 38)(t=8.06,P <0.01).The number of penetrating cells in the visual field of sh-control group(148 ± 19)was significantly higher than that of sh-SCh LAP1 group(67 ± 7)(t=9.77,P <0.01)(4)CCK-8 and flow cytometry showed that the growth curve growth of SCh LAP1-vector group was higher than that of the negative control group,The ratio of apoptosis and the ratio of the S / G2 phase of the cell cycle were also significantly reduced.SCh LAP1 A growth-promoting effect on GBM cell lines.(5)The results of western blot method showed that the HNRNPL protein content in SCh LAP1-vector group was higher than that of the negative control group(t=9.61,P <0.05),and the HNRNPL protein content in sh-SCh LAP1 group was lower than that of the negative control group.The HNRNPL protein content in the SCh LAP1-vector group with the addition of the NF-κB signaling pathway inhibitor was lower than that in the negative control group.Conclusion LncRNA SChLAP1 Promote the proliferation and invasion of GBM cells,and the mechanism may be through the NF-κB signaling pathway.