Background:Oral squamous cell carcinoma(OSCC)is a common malignant tumor.Recently,Laminin Gamma 2(LAMC2)has been shown to be abnormally expressed in OSCC;however,how LAMC2 signaling contributes to the occurrence and d...Background:Oral squamous cell carcinoma(OSCC)is a common malignant tumor.Recently,Laminin Gamma 2(LAMC2)has been shown to be abnormally expressed in OSCC;however,how LAMC2 signaling contributes to the occurrence and development of OSCC and the role of autophagy in OSCC has not been fully explored.This study aimed to analyze the role and mechanism of LAMC2 signaling in OSCC and the involvement of autophagy in OSCC.Methods:To explore the mechanism by which LAMC2 is highly expressed in OSCC,we used small interfering RNA(siRNA)to knock down LAMC2 to further observe the changes in the signaling pathway.Furthermore,we used cell proliferation assays,Transwell invasion assays,and wound-healing assays to observe the changes in OSCC proliferation,invasion,and metastasis.RFP-LC3 was used to detect the level of autophagy intensity.A cell line-derived xenograft(CDX)model was used to detect the effect of LAMC2 on tumor growth in vivo.Results:This study found that the level of autophagy was correlated with the biological behavior of OSCC.The downregulation of LAMC2 activated autophagy and inhibited OSCC proliferation,invasion,and metastasis via inhibiting the PI3K/AKT/mTOR pathway.Moreover,autophagy has a dual effect on OSCC,and the synergistic downregulation of LAMC2 and autophagy can inhibit OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.Conclusions:LAMC2 interacts with autophagy to regulate OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.LAMC2 down-regulation can synergistically modulate autophagy to inhibit OSCC migration,invasion,and proliferation.展开更多
Background:Pancreatic ductal adenocarcinoma(PDAC)poses a serious threat to human health with high mortality and poor prognosis,and there is an urgent need to explore the pathogenesis of PDAC in order to search for new...Background:Pancreatic ductal adenocarcinoma(PDAC)poses a serious threat to human health with high mortality and poor prognosis,and there is an urgent need to explore the pathogenesis of PDAC in order to search for new therapeutic targets.Methods:The expression of lamininγ-2(LAMC2)in PDAC and its effect on the prognosis of tumor patients were predicted by an online database,and the expression level of LAMC2 in pancreatic cancer was verified by polymerase chain reaction(PCR)and western blot;flow cytometry,wound healing assay,Cell counting kit-8(CCK8)assay,and colony formation assay were used to explore the effect of LAMC2 on the proliferation and migration of pancreatic cancer cells;and we also probed the potential relationship between LAMC2 and phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling.Results:High levels of LAMC2 in pancreatic cancer may benefit tumor proliferation migration and invasion and lead to poor prognosis of tumor patients.The mechanism by which LAMC2 promotes PDAC progression may be related to the activation of PI3K/Akt signaling to influence apoptosis and cell cycle.Conclusions:LAMC2 promotes proliferation migration invasion of PDAC and leads to poor prognosis in pancreatic cancer patients.展开更多
基金This work was supported by the National Natural Science Foundation of China(Grant Numbers 31971106,BWS21L013,21WS09002,JK20211A010213).
文摘Background:Oral squamous cell carcinoma(OSCC)is a common malignant tumor.Recently,Laminin Gamma 2(LAMC2)has been shown to be abnormally expressed in OSCC;however,how LAMC2 signaling contributes to the occurrence and development of OSCC and the role of autophagy in OSCC has not been fully explored.This study aimed to analyze the role and mechanism of LAMC2 signaling in OSCC and the involvement of autophagy in OSCC.Methods:To explore the mechanism by which LAMC2 is highly expressed in OSCC,we used small interfering RNA(siRNA)to knock down LAMC2 to further observe the changes in the signaling pathway.Furthermore,we used cell proliferation assays,Transwell invasion assays,and wound-healing assays to observe the changes in OSCC proliferation,invasion,and metastasis.RFP-LC3 was used to detect the level of autophagy intensity.A cell line-derived xenograft(CDX)model was used to detect the effect of LAMC2 on tumor growth in vivo.Results:This study found that the level of autophagy was correlated with the biological behavior of OSCC.The downregulation of LAMC2 activated autophagy and inhibited OSCC proliferation,invasion,and metastasis via inhibiting the PI3K/AKT/mTOR pathway.Moreover,autophagy has a dual effect on OSCC,and the synergistic downregulation of LAMC2 and autophagy can inhibit OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.Conclusions:LAMC2 interacts with autophagy to regulate OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.LAMC2 down-regulation can synergistically modulate autophagy to inhibit OSCC migration,invasion,and proliferation.
基金supported by grants from the National Natural Science Foundation of China(Nos.82171722,82271764,81871954)Beijing Municipal Natural Science Foundation(No.7212111).
文摘Background:Pancreatic ductal adenocarcinoma(PDAC)poses a serious threat to human health with high mortality and poor prognosis,and there is an urgent need to explore the pathogenesis of PDAC in order to search for new therapeutic targets.Methods:The expression of lamininγ-2(LAMC2)in PDAC and its effect on the prognosis of tumor patients were predicted by an online database,and the expression level of LAMC2 in pancreatic cancer was verified by polymerase chain reaction(PCR)and western blot;flow cytometry,wound healing assay,Cell counting kit-8(CCK8)assay,and colony formation assay were used to explore the effect of LAMC2 on the proliferation and migration of pancreatic cancer cells;and we also probed the potential relationship between LAMC2 and phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling.Results:High levels of LAMC2 in pancreatic cancer may benefit tumor proliferation migration and invasion and lead to poor prognosis of tumor patients.The mechanism by which LAMC2 promotes PDAC progression may be related to the activation of PI3K/Akt signaling to influence apoptosis and cell cycle.Conclusions:LAMC2 promotes proliferation migration invasion of PDAC and leads to poor prognosis in pancreatic cancer patients.
