| Background Gastric cancer,as one of the most common malignant tumors,has the third highest mortality in the world.It has complicated pathogenesis,invasion and metastasis mechanism.Its carcinogenesis is a long-term process of cell biological behavior from normal to abnormal.Its pathogenesis is related to many factors,multi-stage and multi gene variation caused by telomerase activation,tumor suppressor gene deactivation and cancer gene activation.In recent years,the overall incidence rate and mortality rate of gastric cancer have been decreasing due to controlling risk factors and screening for gastric cancer.However,due to the huge population base and the aging population,the burden of gastric cancer is still crucial.In China,the incidence rate and related mortality of gastric cancer account for about 50% of the world’s gastric cancer cases.This may be due to the high proportion of advanced gastric cancer at the time of diagnosis.Therefore,it is very important to study the pathogenesis of gastric cancer and reveal biomarkers that can be used for early diagnosis and treatment.At present,the research on Microtubule Associated Serine/Threonine Kinase 3(MAST3)is mainly focused on inflammatory bowel disease.The research shows that cells without mast 3 can reduce the activity of TLR4-dependent NF-κB,which further proves that NF-κB pathway plays an important role in the pathogenesis of inflammatory bowel disease.However,the role and mechanism of MAST3 in the genesis and development of gastric cancer have not been fully understood.The purpose of this study was to observe the expression of MAST3 in gastric cancer and to explore the effect of interference and overexpression of MAST3 on the proliferation and migration of SGC-7901,so as to explore part of the mechanism of gastric cancer and provide theoretical support for early diagnosis and treatment.Objective To explore the effect of Microtubule Associated Serine/Threonine Kinase 3(MAST3)on proliferation and migration in SGC-7901 cells.,and to provide theoretical basis for the prevention,early diagnosis and clinical treatment of gastric cancer.Meterials Western blot and q RT-PCR were used to detect MAST3 expression in gastric cancer tissues.MAST3-RNAi and p Ex-3-MAST3 were further transfected into SGC-7901 cells,and the expressions of Cyclin D1,C-myc,MMP9 and MMP3 were detected by q RT-PCR and Western blot,respectively,observed the effect of MAST3 on the proliferation and migration of SGC-7901 cells.Cell cycle was also detected by flow cytometry.Results(1)The m RNA and protein expression of MAST3 in gastric cancer was significantly higher than that in adjacent tissues by q RT-PCR and Western blot(F = 21.36,P < 0.01;F = 18.76,P < 0.01).The m RNA and protein expression of MAST3 in SGC-7901 cells was up-regulated by TGF-β1 stimulation,and the difference was statistically significant(F = 33.81,P < 0.01;F = 28.71,P < 0.01).(2)The m RNA and protein expression of MAST3 in SGC-7901 cells stimulated by TGF-β1 decreased significantly after transfection of MAST3-RNAi(P < 0.01).After silencing of MAST3-RNAi,C-myc and Cyclin D1 decreased significantly(P < 0.01)The m RNA and protein expression of also decreased significantly in SGC-7901 cells stimulated by TGF-β1,and the difference was statistically significant(P < 0.01).The results of cell cycle also showed that the percentage of S-phase and G2/M-phase cells in MAST3-RNAi group(45 ± 5.2)% was significantly lower than that in NC-RNAi group(65 ± 8.7)% in S-phase and G2/M-phase cells,and the difference was statistically significant(P < 0.05),The expression of m RNA and protein of MMP-3 and MMP-9 was down regulated in SGC-7901 cells stimulated by TGF-β1 silenced by MAST3-RNAi,and the difference was statistically significant(P < 0.01).(3)After transfection with p Ex-3-MAST3,the m RNA and protein expression of MAST3 in SGC-7901 cells stimulated by TGF-β1 was significantly increased(P < 0.01),and the m RNA and protein expression of C-myc and Cyclin D1 in SGC-7901 cells stimulated by TGF-β1 was significantly increased(P < 0.01).The results of cell cycle also showed that the percentage of S-phase and G2/M-phase cells in p Ex-3-MAST3 group(77 ± 4.8)% was higher than that in S-phase and G2/M-phase cells in p Ex-3 group(66 ± 5.1)%,and the difference was statistically significant(P < 0.05).TGF-β1 transfected with p Ex-3-MAST3 stimulated the m RNA and protein expression of MMP-3 and MMP-9 in SGC-7901 cells,and the difference was statistically significant(P < 0.01).Conclusions The results showed that TGF-β1 up-regulated the stimulation of MAST3 in SGC-7901 cells By inhibiting the expression of MAST3,the proliferation and migration of SGC-7901 cells can be inhibited,while up-regulating the expression of MAST3 can increase the proliferation and migration of SGC-7901 cells,which indicates that MAST3 can regulate the proliferation and migration of SGC-7901 cells,which is closely related to the occurrence of gastric cancer. |
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