目的观察正常和不同病变程度的口腔黏膜上皮细胞对α干扰素(IFN-α)敏感性的差异,为IFN-α的抗肿瘤应用和机制的研究提供基础。方法分别培养正常口腔黏膜上皮细胞株(NOK)、口腔黏膜异常增生上皮细胞株(DOK)、口腔表皮样癌细胞株(KB),取...目的观察正常和不同病变程度的口腔黏膜上皮细胞对α干扰素(IFN-α)敏感性的差异,为IFN-α的抗肿瘤应用和机制的研究提供基础。方法分别培养正常口腔黏膜上皮细胞株(NOK)、口腔黏膜异常增生上皮细胞株(DOK)、口腔表皮样癌细胞株(KB),取传至第3代对数生长期细胞接种于细胞培养板,对照组每孔加入2 m L含10%胎牛血清的完全培养液,实验组设IFN-α浓度100、500、1 000 U/m L 3个浓度组,实验组每孔分别加入含相应浓度IFN-α的完全培养液,常规培养24 h后检测细胞增殖能力、细胞凋亡和细胞周期变化情况。结果不同浓度的IFN-α分别作用于3种细胞,对NOK细胞株的增殖能力无影响,而DOK、KB细胞株各实验组与对照组相比增殖能力明显减慢,差异均有显著统计学意义(均P<0.01)。浓度500 U/m L IFN-α对NOK细胞株的凋亡无影响,但有促进DOK、KB细胞株凋亡的作用。浓度500 U/m L IFN-α对NOK细胞株周期无影响,DOK细胞株G0/G1期细胞比例显著减少,而G2/M期细胞比例显著增加,KB细胞株G2/M期细胞比例显著增加。结论正常上皮细胞对IFN-α不敏感,而DOK、KB细胞株对IFN-α敏感;IFN-α有抑制DOK、KB细胞株的增殖能力、促其凋亡的作用,且细胞周期阻滞于G2/M期。展开更多
Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti...Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti-HBV effects of IFN-α are less reported. Here we show that CK1α can interact with IFNAR1 in hepatoma carcinoma cells and increased the abundance of IFNAR1 by reducing the ubiquitination levels in the presence of HBV.Furthermore, CK1α promotes the IFN-α triggered JAK-STAT signaling pathway and consequently enhances the antiviral effects of IFN-α against HBV replication. Our results collectively provide evidence that CK1α positively regulates the anti-HBV activity of IFN-α in hepatoma carcinoma cells, which would be a promising therapeutic target to improve the effectiveness of IFN-α therapy to cure CHB.展开更多
A novel way for photo-immobilization with interferon- α（IFN- α） on the surface of polyurethane （PU） material, which makes PU condom more effective function in the future, was investigated. A kind of photoactive ...A novel way for photo-immobilization with interferon- α（IFN- α） on the surface of polyurethane （PU） material, which makes PU condom more effective function in the future, was investigated. A kind of photoactive arylazide-4-azidobenzoic acid was modified to IFN- α with the confirmation of IR and Raman spectrum. Micro morphology of the photo-immobilized cell factors was observed by FESEM as well as CSLM at the level of nanometer. Finally, the product with elementary test of anti-microbial was also evaluated.展开更多
Hepatocarcinoma is one of the malignant cancers with significant morbidity and mortality.Immunotherapy has emerged in clinical treatment,owing to the limitation and severe side effects of chemotherapy.In the immune sy...Hepatocarcinoma is one of the malignant cancers with significant morbidity and mortality.Immunotherapy has emerged in clinical treatment,owing to the limitation and severe side effects of chemotherapy.In the immune system,natural killer（NK）cells are important effectors required to eliminate malignant tumor cells without the limitation of major histocompatibility complex（MHC）molecule issues.Hence,treatment which could stimulate NK cells is of great interest.Here,we investigated the efficacy of the combined therapy of TT-1（a mutant of melittin）and interferon-α（IFN-α）on NK cells and human liver cancer HepG-2/Huh7 cells in vitro and in vivo,as well as the mechanism involved.The combination therapy significantly inhibited the growth of HepG-2/Huh7 cells in vivo,but this effect was impaired after depleting NK cells.TT-1 not only up-regulated MHC class I-related chain molecules A（MICA）expression,but also prevented the secretion of soluble MICA（sM ICA）.Both the mR NA and protein of a disintegrin and metallopeptidase 10（ADAM 10）in HepG-2/Huh7 cells were decreased after TT-1 treatment.The combined therapy of TT-1 and IFN-αcould suppress the growth of HepG-2/Huh7 xenografted tumor effectively via promoting the interaction of NK group 2,member D（NKG2D）and MICA,indicating that TT-1＋IFN-αwould be a potential approach in treating liver cancer.展开更多
文摘目的观察正常和不同病变程度的口腔黏膜上皮细胞对α干扰素(IFN-α)敏感性的差异,为IFN-α的抗肿瘤应用和机制的研究提供基础。方法分别培养正常口腔黏膜上皮细胞株(NOK)、口腔黏膜异常增生上皮细胞株(DOK)、口腔表皮样癌细胞株(KB),取传至第3代对数生长期细胞接种于细胞培养板,对照组每孔加入2 m L含10%胎牛血清的完全培养液,实验组设IFN-α浓度100、500、1 000 U/m L 3个浓度组,实验组每孔分别加入含相应浓度IFN-α的完全培养液,常规培养24 h后检测细胞增殖能力、细胞凋亡和细胞周期变化情况。结果不同浓度的IFN-α分别作用于3种细胞,对NOK细胞株的增殖能力无影响,而DOK、KB细胞株各实验组与对照组相比增殖能力明显减慢,差异均有显著统计学意义(均P<0.01)。浓度500 U/m L IFN-α对NOK细胞株的凋亡无影响,但有促进DOK、KB细胞株凋亡的作用。浓度500 U/m L IFN-α对NOK细胞株周期无影响,DOK细胞株G0/G1期细胞比例显著减少,而G2/M期细胞比例显著增加,KB细胞株G2/M期细胞比例显著增加。结论正常上皮细胞对IFN-α不敏感,而DOK、KB细胞株对IFN-α敏感;IFN-α有抑制DOK、KB细胞株的增殖能力、促其凋亡的作用,且细胞周期阻滞于G2/M期。
基金supported by the National Key Research and Development Program of China(2018YFE0107500)the Natural Science Foundation Project of Science and Technology Agency of Chongqing YuZhong District(20200122)to Hu Yuana Natural Science Foundation Project of CQ CSTC(cstc2021jcyj-msxmX0276)to Chen YanMeng
文摘Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti-HBV effects of IFN-α are less reported. Here we show that CK1α can interact with IFNAR1 in hepatoma carcinoma cells and increased the abundance of IFNAR1 by reducing the ubiquitination levels in the presence of HBV.Furthermore, CK1α promotes the IFN-α triggered JAK-STAT signaling pathway and consequently enhances the antiviral effects of IFN-α against HBV replication. Our results collectively provide evidence that CK1α positively regulates the anti-HBV activity of IFN-α in hepatoma carcinoma cells, which would be a promising therapeutic target to improve the effectiveness of IFN-α therapy to cure CHB.
基金Funded by the Guangdong Technology Projects (No.2006B35802003)the Natural Science Foundation of Guangdong Province (No.8451063101000345)the Opening Project of MOE Key laboratory of Laser Life Science, South China Normal University, Guangzhou 510631, China
文摘A novel way for photo-immobilization with interferon- α（IFN- α） on the surface of polyurethane （PU） material, which makes PU condom more effective function in the future, was investigated. A kind of photoactive arylazide-4-azidobenzoic acid was modified to IFN- α with the confirmation of IR and Raman spectrum. Micro morphology of the photo-immobilized cell factors was observed by FESEM as well as CSLM at the level of nanometer. Finally, the product with elementary test of anti-microbial was also evaluated.
基金supported by the Outstanding Young Talent Foundation Project of Science and Technology Department in Jilin Province(No.20170520018JH),China
文摘Hepatocarcinoma is one of the malignant cancers with significant morbidity and mortality.Immunotherapy has emerged in clinical treatment,owing to the limitation and severe side effects of chemotherapy.In the immune system,natural killer（NK）cells are important effectors required to eliminate malignant tumor cells without the limitation of major histocompatibility complex（MHC）molecule issues.Hence,treatment which could stimulate NK cells is of great interest.Here,we investigated the efficacy of the combined therapy of TT-1（a mutant of melittin）and interferon-α（IFN-α）on NK cells and human liver cancer HepG-2/Huh7 cells in vitro and in vivo,as well as the mechanism involved.The combination therapy significantly inhibited the growth of HepG-2/Huh7 cells in vivo,but this effect was impaired after depleting NK cells.TT-1 not only up-regulated MHC class I-related chain molecules A（MICA）expression,but also prevented the secretion of soluble MICA（sM ICA）.Both the mR NA and protein of a disintegrin and metallopeptidase 10（ADAM 10）in HepG-2/Huh7 cells were decreased after TT-1 treatment.The combined therapy of TT-1 and IFN-αcould suppress the growth of HepG-2/Huh7 xenografted tumor effectively via promoting the interaction of NK group 2,member D（NKG2D）and MICA,indicating that TT-1＋IFN-αwould be a potential approach in treating liver cancer.
