BACKGROUND Gastric cancer(GC)is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency,but its exact pathogenesis has not been fully elucidated.ETS ho...BACKGROUND Gastric cancer(GC)is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency,but its exact pathogenesis has not been fully elucidated.ETS homologous factor(EHF)is an important member of the ETS family and contributes to the pathogenesis of multiple malignant tumors.To date,whether EHF participates in the development of GC via the c-Met signaling pathway remains unclear.AIM To investigate the role and mechanism of EHF in the occurrence and development of GC.METHODS The expression of EHF mRNA in GC tissues and cell lines was measured by quantitative PCR.Western blotting was performed to determine the protein expression of EHF,c-Met,and its downstream signal molecules.The EHF expression in GC tissues was further detected by immunohistochemical staining.To investigate the role of EHF in GC oncogenesis,small interfering RNA(siRNA)against EHF was transfected into GC cells.The cell proliferation of GC cells was determined by Cell Counting Kit-8 and colony formation assays.Flow cytometry was performed following Annexin V/propidium iodide(PI)to identify apoptotic cells and PI staining to analyze the cell cycle.Cell migration and invasion were assessed by transwell assays.RESULTS The data showed that EHF was upregulated in GC tissues and cell lines in which increased expression of c-Met was also observed.Silencing of EHF by siRNA reduced the proliferation of GC cells.Inhibition of EHF induced significant apoptosis and cell cycle arrest in GC cells.Cell migration and invasion were significantly inhibited.EHF silencing led to c-Met downregulation and further blocked the Ras/c-Raf/extracellular signal-related kinase 1/2(Erk1/2)pathway.Additionally,phosphatase and tensin homolog was upregulated and glycogen synthase kinase 3 beta was deactivated.Moreover,inactivation of signal transducer and activator of transcription 3 was detected following EHF inhibition,leading to inhibition of the epithelial-to-mesenchymal transition(EMT).CONCLUSION These results suggest that EHF plays a key role in cell proliferation,invasion,apoptosis,the cell cycle and EMT via the c-Met pathway.Therefore,EHF may serve as an antineoplastic target for the diagnosis and treatment of GC.展开更多
[Objective]The aim was to select the suitable hormone factors for flowering induction in vitro culture of Dendrobium officinate Kimura et Migo.[Method]The test-tube plantlets from the stems of Dendrobium officinate Ki...[Objective]The aim was to select the suitable hormone factors for flowering induction in vitro culture of Dendrobium officinate Kimura et Migo.[Method]The test-tube plantlets from the stems of Dendrobium officinate Kimura et Migo were used as the experimental materials and MS medium as the basic medium.Comparative tests have been done between single-factor hormone treatments（different concentrations of PP333 or TDZ） and multi-factor hormone treatments（different combinations of PP333,TDZ,6-BA and NAA） to research the effects of hormone factors on the flowering induction of the plantlets.[Result]Among the single-factor hormone treatments,the suitable concentration and the rate of flower buds formation of PP333 treatment were 0.2 mg/L and 8.5%,the that of TDZ treatment were 0.06 mg/L and 15.5%;the effects of multi-factor hormone treatments on the flowering induction were ordered as follow：（PP333 ＋ 6-BA ＋ NAA ＋ TDZ）〉 （PP333 ＋ 6-BA ＋ NAA）〉 （PP333 ＋ 6-BA） and（PP333 ＋ NAA） ;the most suitable treatment was PP333 0.3 mg/L ＋ 6-BA 0.5 mg/L ＋ NAA 0.5 mg/L ＋ TDZ 0.06 mg/L,the rate of flower bud formation and the rate of the blossomed flower were respectly reached to 80.4% and 90.3%.[Conclusion]PP333 and TDZ showed the important effect on the flowering induction in vitro culture of Dendrobium officinate Kimura et Migo.The effect of TDZ was better than that of PP333.It is much more conducive to the flower bud formation,when using appropriate concentration of TDZ combined with other hormones properly.展开更多
基金Supported by The Traditional Chinese Medicine Science and Technology Plan of Zhejiang Province,No.2017ZZ010Zhejiang Medical Science and Technology Program,No.2018266817.
文摘BACKGROUND Gastric cancer(GC)is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency,but its exact pathogenesis has not been fully elucidated.ETS homologous factor(EHF)is an important member of the ETS family and contributes to the pathogenesis of multiple malignant tumors.To date,whether EHF participates in the development of GC via the c-Met signaling pathway remains unclear.AIM To investigate the role and mechanism of EHF in the occurrence and development of GC.METHODS The expression of EHF mRNA in GC tissues and cell lines was measured by quantitative PCR.Western blotting was performed to determine the protein expression of EHF,c-Met,and its downstream signal molecules.The EHF expression in GC tissues was further detected by immunohistochemical staining.To investigate the role of EHF in GC oncogenesis,small interfering RNA(siRNA)against EHF was transfected into GC cells.The cell proliferation of GC cells was determined by Cell Counting Kit-8 and colony formation assays.Flow cytometry was performed following Annexin V/propidium iodide(PI)to identify apoptotic cells and PI staining to analyze the cell cycle.Cell migration and invasion were assessed by transwell assays.RESULTS The data showed that EHF was upregulated in GC tissues and cell lines in which increased expression of c-Met was also observed.Silencing of EHF by siRNA reduced the proliferation of GC cells.Inhibition of EHF induced significant apoptosis and cell cycle arrest in GC cells.Cell migration and invasion were significantly inhibited.EHF silencing led to c-Met downregulation and further blocked the Ras/c-Raf/extracellular signal-related kinase 1/2(Erk1/2)pathway.Additionally,phosphatase and tensin homolog was upregulated and glycogen synthase kinase 3 beta was deactivated.Moreover,inactivation of signal transducer and activator of transcription 3 was detected following EHF inhibition,leading to inhibition of the epithelial-to-mesenchymal transition(EMT).CONCLUSION These results suggest that EHF plays a key role in cell proliferation,invasion,apoptosis,the cell cycle and EMT via the c-Met pathway.Therefore,EHF may serve as an antineoplastic target for the diagnosis and treatment of GC.
基金Supported by Plan Project of Science and Technology Committee of Guangxi Province (0322024-3A) Scientific Research Foundation for Returned Scholars of Guangxi Province~~
文摘[Objective]The aim was to select the suitable hormone factors for flowering induction in vitro culture of Dendrobium officinate Kimura et Migo.[Method]The test-tube plantlets from the stems of Dendrobium officinate Kimura et Migo were used as the experimental materials and MS medium as the basic medium.Comparative tests have been done between single-factor hormone treatments（different concentrations of PP333 or TDZ） and multi-factor hormone treatments（different combinations of PP333,TDZ,6-BA and NAA） to research the effects of hormone factors on the flowering induction of the plantlets.[Result]Among the single-factor hormone treatments,the suitable concentration and the rate of flower buds formation of PP333 treatment were 0.2 mg/L and 8.5%,the that of TDZ treatment were 0.06 mg/L and 15.5%;the effects of multi-factor hormone treatments on the flowering induction were ordered as follow：（PP333 ＋ 6-BA ＋ NAA ＋ TDZ）〉 （PP333 ＋ 6-BA ＋ NAA）〉 （PP333 ＋ 6-BA） and（PP333 ＋ NAA） ;the most suitable treatment was PP333 0.3 mg/L ＋ 6-BA 0.5 mg/L ＋ NAA 0.5 mg/L ＋ TDZ 0.06 mg/L,the rate of flower bud formation and the rate of the blossomed flower were respectly reached to 80.4% and 90.3%.[Conclusion]PP333 and TDZ showed the important effect on the flowering induction in vitro culture of Dendrobium officinate Kimura et Migo.The effect of TDZ was better than that of PP333.It is much more conducive to the flower bud formation,when using appropriate concentration of TDZ combined with other hormones properly.
