2015年4月21日上午,在泰勒霍普森CIMT2015的展台上,本刊记者又见到了老朋友——泰勒霍普森中国区总经理曾理先生,同时,他还为本刊记者介绍了一位新朋友——Neil B Curtis先生,泰勒霍普森销售总监。曾总风采依旧,欢笑更胜。坐下细聊方知...2015年4月21日上午,在泰勒霍普森CIMT2015的展台上,本刊记者又见到了老朋友——泰勒霍普森中国区总经理曾理先生,同时,他还为本刊记者介绍了一位新朋友——Neil B Curtis先生,泰勒霍普森销售总监。曾总风采依旧,欢笑更胜。坐下细聊方知,＂喜＂出有因。展开更多
Objective:To explore the genetic changes in the progression of castration-resistant prostate cancer(CRPC)and neuroendocrine prostate cancer(NEPC)and the reason why these cancers resist existing therapies.Methods:We em...Objective:To explore the genetic changes in the progression of castration-resistant prostate cancer(CRPC)and neuroendocrine prostate cancer(NEPC)and the reason why these cancers resist existing therapies.Methods:We employed our CRPC cell line microarray and other CRPC or NEPC datasets to screen the target gene NEIL3.Lentiviral transfection and RNA interference were used to construct overexpression and knockdown cell lines.Cell and animal models of radiotherapy were established by using a medical electron linear accelerator.Flow cytometry was used to detect apoptosis or cell cycle progression.Western blot and qPCR were used to detect changes in the protein and RNA levels.Results:TCGA and clinical patient datasets indicated that NEIL3 was downregulated in CRPC and NEPC cell lines,and NEIL3 was correlated with a high Gleason score but a good prognosis.Further functional studies demonstrated that NEIL3 had no effect on the proliferation and migration of PCa cells.However,cell and animal radiotherapy models revealed that NEIL3 could facilitate the radiotherapy sensitivity of PCa cells,while loss of NEIL3 activated radiotherapy resistance.Mechanistically,we found that NEIL3 negatively regulated the expression of ATR,and higher NEIL3 expression repressed the ATR/CHK1 pathway,thus regulating the cell cycle.Conclusions:We demonstrated that NEIL3 may serve as a diagnostic or therapeutic target for therapy-resistant patients.展开更多
AIM:To identify genetic polymorphisms in the promoter region of the human base excision repair gene NEIL1 in gastric cancer patients.METHODS:The NEIL1 promoter region in DNA from 80 Japanese patients with gastric canc...AIM:To identify genetic polymorphisms in the promoter region of the human base excision repair gene NEIL1 in gastric cancer patients.METHODS:The NEIL1 promoter region in DNA from 80 Japanese patients with gastric cancer was searched for genetic polymorphisms by polymerase chain reaction-single-strand conformation polymorphism and subsequent sequencing analyses.RESULTS:Three novel genetic polymorphisms,i.e.c.-3769C>T,c.-3170T>G,and c.-2681TA[8],were identified in the NEIL1 promoter region at an allele frequency of 0.6%,9.4%,and 4.4%,respectively,in Japanese gastric cancer patients.CONCLUSION:Three NEIL1 promoter polymorphisms detected in this study may be of importance in gastric carcinogenesis.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.81672550 and 81974395)Guangdong Basic and Applied Basic Research Foundation(Grant No.2019A1515011437)+4 种基金Guangzhou Science and Technology Cooperation Program(Foreign Research and Development Cooperation)(Grant No.201807010087)Clinical Research 5010 Program of Sun Yat-sen University(Grant No.2019005)Sun Yat-Sen Clinical Research and Cultivation Project of Sun Yat Sen University(Grant No.201702)to Hai Huangsupported by the National Natural Science Foundation of China(Grant No.81702527)supported by the China Scholarship Council(Grant No.201906380075).
文摘Objective:To explore the genetic changes in the progression of castration-resistant prostate cancer(CRPC)and neuroendocrine prostate cancer(NEPC)and the reason why these cancers resist existing therapies.Methods:We employed our CRPC cell line microarray and other CRPC or NEPC datasets to screen the target gene NEIL3.Lentiviral transfection and RNA interference were used to construct overexpression and knockdown cell lines.Cell and animal models of radiotherapy were established by using a medical electron linear accelerator.Flow cytometry was used to detect apoptosis or cell cycle progression.Western blot and qPCR were used to detect changes in the protein and RNA levels.Results:TCGA and clinical patient datasets indicated that NEIL3 was downregulated in CRPC and NEPC cell lines,and NEIL3 was correlated with a high Gleason score but a good prognosis.Further functional studies demonstrated that NEIL3 had no effect on the proliferation and migration of PCa cells.However,cell and animal radiotherapy models revealed that NEIL3 could facilitate the radiotherapy sensitivity of PCa cells,while loss of NEIL3 activated radiotherapy resistance.Mechanistically,we found that NEIL3 negatively regulated the expression of ATR,and higher NEIL3 expression repressed the ATR/CHK1 pathway,thus regulating the cell cycle.Conclusions:We demonstrated that NEIL3 may serve as a diagnostic or therapeutic target for therapy-resistant patients.
基金Supported by Grants-in-Aid from Ministry of Health, Labour and Welfare for the Comprehensive 10-Year Strategy for Cancer Control (19-19)Japan Society for the Promotion of Science for Scientific Research, No. 19790286+1 种基金Ministry of Education, Culture,Sports, Science and Technology for priority area, No. 20014007the 21st century COE program
文摘AIM:To identify genetic polymorphisms in the promoter region of the human base excision repair gene NEIL1 in gastric cancer patients.METHODS:The NEIL1 promoter region in DNA from 80 Japanese patients with gastric cancer was searched for genetic polymorphisms by polymerase chain reaction-single-strand conformation polymorphism and subsequent sequencing analyses.RESULTS:Three novel genetic polymorphisms,i.e.c.-3769C>T,c.-3170T>G,and c.-2681TA[8],were identified in the NEIL1 promoter region at an allele frequency of 0.6%,9.4%,and 4.4%,respectively,in Japanese gastric cancer patients.CONCLUSION:Three NEIL1 promoter polymorphisms detected in this study may be of importance in gastric carcinogenesis.
