Correction to “Interleukin-34 promotes the proliferation and epithelial-mesenchymal transition of gastric cancer cells”

Correction to“Interleukin-34 promotes the proliferation and epithelialmesenchymal transition of gastric cancer cells”.In this article,we found the following error in Figure 3A:The panel image"24 h,sh-RNA1"in the AGS cells wound healing assay was incorrectly inserted during the preparation of the submission;the correct figure is provided in this correction.

Cryptotanshinone inhibits cytotoxin-associated gene A-associated development of gastric cancer and mucosal erosions

BACKGROUND Approximately 90%of new cases of noncardiac gastric cancer(GC)are related to Helicobacter pylori(H.pylori),and cytotoxin-associated gene A(CagA)is one of the main pathogenic factors.Recent studies have shown that the pharmacological effects of cryptotanshinone(CTS)can be used to treat a variety of tumors.However,the effects of CTS on H.pylori,especially CagA+strain-induced gastric mucosal lesions,on the development of GC is unknown.AIM To assess the role of CTS in CagA-induced proliferation and metastasis of GC cells,and determine if CagA+H.pylori strains causes pathological changes in the gastric mucosa of mice.METHODS The effects of CTS on the proliferation of GC cells were assessed using the Cell Counting Kit-8(CCK-8)assay,and the abnormal growth,migration and invasion caused by CagA were detected by CCK-8 and transwell assays.After transfection with pSR-HA-CagA and treatment with CTS,proliferation and metastasis were evaluated by CCK-8 and transwell assays,respectively,and the expression of Src homology 2(SH2)domain–containing phosphatase 2(SHP2)and phosphorylated SHP2(p-SHP2)was detected using western blotting in AGS cells.The enzymelinked immunosorbent assay was used to determine the immunoglobulin G(IgG)level against CagA in patient serum.Mice were divided into four groups and administered H.pylori strains(CagA+or CagA-)and CTS(or PBS)intragastrically,and establishment of the chronic infection model was verified using polymerase chain reaction and sequencing of isolated strains.Hematoxylin and eosin staining was used to assess mucosal erosion in the stomach and toxicity to the liver and kidney.RESULTS CTS inhibited the growth of GC cells in dose-and time-dependent manners.Overexpression of CagA promoted the growth,migration,and invasion of GC cells.Importantly,we demonstrated that CTS significantly inhibited the CagAinduced abnormal proliferation,migration,and invasion of GC cells.Moreover,the expression of p-SHP2 protein in tumor tissue was related to the expression of IgG against CagA in the serum of GC patients.Additionally,CTS suppressed the protein expression levels of both SHP2 and p-SHP2 in GC cells.CTS suppressed CagA+H.pylori strain-induced mucosal erosion in the stomach of mice but had no obvious effects on the CagA-H.pylori strain group.CONCLUSION CTS inhibited CagA-induced proliferation and the epithelial-mesenchymal transition of GC cells in vitro,and CagA+H.pylori strains caused mucosal erosions of the stomach in vivo by decreasing the protein expression of SHP2.

Interleukin-34 promotes the proliferation and epithelial-mesenchymal transition of gastric cancer cells

BACKGROUND Interleukin(IL)-34 is a pro-inflammatory cytokine involved in tumor development.The role of IL-34 in the proliferation and epithelial-mesenchymal transition(EMT)of gastric cancer(GC)remains to be investigated.AIM To investigate whether and how IL-34 affects the proliferation of GC cells and EMT.METHODS Using immunohistochemical staining,the expression of IL-34 protein was detected in 60 paired GC and normal paracancerous tissues and the relationship between IL-34 and clinicopathological factors was analyzed.The expression of IL-34 mRNA and protein in normal gastric epithelial cell lines and GC was detected using quantitative real-time polymerase chain reaction(qRT-PCR)and western blotting,respectively.Stable IL-34 knockdown and overexpression in AGS cell lines were established by lentiviral infection and validated by qRT-PCR and western blotting.The cholecystokinin-8 assay,clone formation assay,cell scratch assay,and transwell system were used to detect GC cell proliferation,clone formation,migration,and invasion capacity,respectively.The effects of IL-34 on the growth of GC transplant tumors were assessed using a subcutaneous transplant tumor assay in nude mice.The effects of IL-34 on the expression level of EMT-associated proteins in AGS cells were examined by western blotting.RESULTS Expression of IL-34 protein and mRNA was higher in GC cell lines than in GES-1 cells.Compared to matched normal paraneoplastic tissues,the expression of IL-34 protein was higher in 60 GC tissues,which was correlated with tumor size,T-stage,N-stage,tumor,node and metastasis stage,and degree of differentiation.Knockdown of IL-34 expression inhibited the proliferation,clone formation,migration,and invasion of AGS cells,while overexpression of IL-34 promoted cell proliferation,clone formation,migration,and invasion.Furthermore,the reduction of IL-34 promoted the expression of E-cadherin in AGS cells but inhibited the expression of vimentin and N-cadherin.Overexpression of IL-34 inhibited E-cadherin expression but promoted expression of vimentin and N-cadherin in AGS cells.Overexpression of IL-34 promoted the growth of subcutaneous transplanted tumors in nude mice.CONCLUSION IL-34 expression is increased in GC tissues and cell lines compared to normal gastric tissues or cell lines.In GC cells,IL-34 promoted proliferation,clone formation,migration,and invasion by regulating EMT-related protein expression cells.Interference with IL-34 may represent a novel strategy for diagnosis and targeted therapy of GC.