The Role And Mechanism Of CD36 Molecule In Invasion,Metastasis,and Lipid Metabolism Of Pancreatic Cancer

Objective In this study,bioinformatics analysis was used to predict the biological functions of CD36 molecule.Then,CD36 cell model was constructed to explore the influence of CD36 molecule on the growth,proliferation,invasion and migration of pancreatic cancer cells,and the relationship between CD36 and lipid metabolism was also discussed.The effect of CD36 on tumor cell related signaling pathway proteins was further investigated.This study will provide theoretical basis for subsequent biological experiments,provide a new plan for clinical treatment of pancreatic tumors,and promote the study of CD36 on the mechanism of tumor genesis and development.Methods 1.Bioinformatics analysis.2.Western blot and RT-PCR experiments were used to detect the expression of CD36 in pancreatic cancer cells and endothelial cells.3.CD36 lentivirus was transfected into pancreatic cancer tumor cells,and a cell model with stable knockdown of CD36 and overexpression of CD36 was constructed.4.Western blot assay was used to detect the effect of CD36 lentivirus transfection and related signaling pathways.5.The effect of CD36 molecule on the growth and proliferation of tumor cells was detected by EdU-594 cell proliferation assay and cell clone formation assay.6.The effect of CD36 molecule on tumor cell invasion and migration ability was detected by Transwell invasion assay and scratch assay.7.HE staining was used to compare the difference between human pancreatic cancer tumor tissue and adjacent normal tissue.8.Immunohistochemistry were used to compare the expression of CD36 in human pancreatic cancer tumor tissue and adjacent normal tissue.9.RT-PCR were used to detecte the change of lipid metabolism-related gene expression before and after CD36 lentivirus transfection.10.Oil red O staining to compare the lipid content of pancreatic cancer cells before and after CD36 lentivirus transfection.11.BODIP Y staining to compare the content of lipid droplets in pancreatic cancer cells before and after CD36 lentivirus transfection.Results 1.The results of bioinformatics analysis showed that compared with normal pancreatic tissue,the expression of CD36 molecule in pancreatic cancer was low,and the expression of CD36 was positively correlated with several immune cells.The results of KEGG-GO analysis showed that CD36 was involved in various regulatory pathways and regulated multiple biological functions.2.Western blot and RT-PCR results showed that CD36 was up-regulated in pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells.3.The results of EdU-594 cell proliferation experiments showed that the proliferation of pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells was weakened after CD3 6 knockdown.4.The results of cell colony formation experiments showed that compared with the control group,the colony formation ability of pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells decreased after CD36 knockdown.Western blot results showed that after CD36 knockdown,AKT protein phosphorylation was inhibited and EGFR protein expression was down-regulated in pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells.5.The results of Transwell invasion assay and cell scratch assay showed that compared with the control group,the ability of pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells to invade and migrate was weakened after CD3 6 knockdown.Western blot results showed that the expression of p-ERK and MMP-9 proteins in pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells decreased after CD36 knockdown.6.The results of immunohistochemistry showed that the expression of CD36 was down-regulated in tumor tissue compared with normal pancreatic tissue.7.RT-PCR results showed that CD36 molecule was involved in lipid metabolism,and the expression of lipid metabolism-related genes in pancreatic cancer cells decreased after CD36 molecule knockdown.In pancreatic cancer cells overexpressing CD36 molecule,the expression of ApoE and AC AT1 genes was significantly up-regulated.8.Oil red O staining and BODIPY 493/503 staining results showed that the lipid content and accumulation of lipids in overexpressed CD36 pancreatic cancer cells increased.Conclusion 1.Inhibition the expression of CD36 protein in pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells could attenuate tumor cell proliferation and clone formation.2.Inhibiting the expression of CD36 protein in pancreatic cancer PANC-1 cells,BxPC-3 cells and MiaPaCa-2 cells could attenuate the invasion and migration ability of tumor cells.3.CD36 molecule is involved in tumor lipid metabolism,and pancreatic cancer cells overexpressing CD36 molecule have increased lipid absorption and lipid accumulation.