This editorial reviews the molecular mechanisms underlying the roles of the long non-coding RNA(lncRNA)small nucleolar RNA host gene 16(SNHG16)in digestive system cancers based on two recent studies on lncRNAs in dige...This editorial reviews the molecular mechanisms underlying the roles of the long non-coding RNA(lncRNA)small nucleolar RNA host gene 16(SNHG16)in digestive system cancers based on two recent studies on lncRNAs in digestive system tumors.The first study,by Zhao et al,explored how hBD-1 affects colon cancer,via the lncRNA TCONS_00014506,by inhibiting mTOR and promoting autophagy.The second one,by Li et al,identified the lncRNA prion protein testis specific(PRNT)as a factor in oxaliplatin resistance by sponging ZNF184 to regulate HIPK2 and influence colorectal cancer progression and chemoresistance,suggesting PRNT as a potential therapeutic target for colorectal cancer.Both of these two articles discuss the mechanisms by which lncRNAs contribute to the development and progression of digestive system cancers.As a recent research hotspot,SNHG16 is a typical lncRNA that has been extensively studied for its association with digestive system cancers.The prevailing hypothesis is that SNHG16 participates in the development and progression of digestive system tumors by acting as a competing endogenous RNA,interacting with other proteins,regulating various genes,and affecting downstream target molecules.This review systematically examines the recently reported biological functions,related molecular mechanisms,and potential clinical significance of SNHG16 in various digestive system cancers,and explores the relationship between SNHG16 and digestive system cancers.The findings suggest that SNHG16 may serve as a potential biomarker and therapeutic target for human digestive system cancers.展开更多
Cancer has become the most life-threatening disease in the world.Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs,especially long noncoding RNAs(lncRNAs),have significant...Cancer has become the most life-threatening disease in the world.Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs,especially long noncoding RNAs(lncRNAs),have significant effects in human cancers.LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes.Small nucleolar RNA host gene 3(SNHG3)is a novel lncRNA and has been reported to be differentially expressed in various tumors,such as liver cancer,gastric cancer,and glioma.However,the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood.In this review,we summarize the results of SNHG3 studies in humans,animal models,and cells to underline the expression and role of SNHG3 in cancer.SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis.SNHG3 expression in lung adenocarcinoma remains controversial.Concurrently,SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms,including competing endogenous RNA effects.A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.展开更多
Objective： To investigate the role of Spl as transcription factor required for transactivation of LRP16 gene by estrogen. Methods： Specific antibodies of ERα and Spl were used to precipitate the target DNA/protein...Objective： To investigate the role of Spl as transcription factor required for transactivation of LRP16 gene by estrogen. Methods： Specific antibodies of ERα and Spl were used to precipitate the target DNA/protein complexes of MCF-7 cells at different time points after estrogen treatment （Chromatin immunoprecipitation assay）, the promoter region of LRP16 gene was amplified by semi-nested polymerase chain reaction （snPCR）. Small interfering RNA （siRNA） against Spl was transiently cotransfected with LRP16-Luc （containing the region from -213bp to -126bp of LRP16 gene promoter）in MCF-7 cells. The luciferase activities were measured by dual-luciferase assay. Results： The results of chromatin immunoprecipitation assay showed that Spl protein directly bound to the -213bp to -126bp region of LRP16 gene, and ERα could enhance the affinity of Spl to DNA. Spl-siRNA specifically decreased the transactivation of LRP16-Luc by 1713-estradio1 to 70-80%. Conclusion： The estrogen-induced transactivation of the human LRP16 gene was mediated by Spl protein. Moreover, the interactions of ERα/Sp1 functional complex with LRP16 promoter DNA were required for enhanced LRP16 gene transactivation.展开更多
文摘This editorial reviews the molecular mechanisms underlying the roles of the long non-coding RNA(lncRNA)small nucleolar RNA host gene 16(SNHG16)in digestive system cancers based on two recent studies on lncRNAs in digestive system tumors.The first study,by Zhao et al,explored how hBD-1 affects colon cancer,via the lncRNA TCONS_00014506,by inhibiting mTOR and promoting autophagy.The second one,by Li et al,identified the lncRNA prion protein testis specific(PRNT)as a factor in oxaliplatin resistance by sponging ZNF184 to regulate HIPK2 and influence colorectal cancer progression and chemoresistance,suggesting PRNT as a potential therapeutic target for colorectal cancer.Both of these two articles discuss the mechanisms by which lncRNAs contribute to the development and progression of digestive system cancers.As a recent research hotspot,SNHG16 is a typical lncRNA that has been extensively studied for its association with digestive system cancers.The prevailing hypothesis is that SNHG16 participates in the development and progression of digestive system tumors by acting as a competing endogenous RNA,interacting with other proteins,regulating various genes,and affecting downstream target molecules.This review systematically examines the recently reported biological functions,related molecular mechanisms,and potential clinical significance of SNHG16 in various digestive system cancers,and explores the relationship between SNHG16 and digestive system cancers.The findings suggest that SNHG16 may serve as a potential biomarker and therapeutic target for human digestive system cancers.
基金Supported by the National Science and Technology Major Project of China,No. 2018ZX10302206 and 2017ZX10202203
文摘Cancer has become the most life-threatening disease in the world.Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs,especially long noncoding RNAs(lncRNAs),have significant effects in human cancers.LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes.Small nucleolar RNA host gene 3(SNHG3)is a novel lncRNA and has been reported to be differentially expressed in various tumors,such as liver cancer,gastric cancer,and glioma.However,the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood.In this review,we summarize the results of SNHG3 studies in humans,animal models,and cells to underline the expression and role of SNHG3 in cancer.SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis.SNHG3 expression in lung adenocarcinoma remains controversial.Concurrently,SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms,including competing endogenous RNA effects.A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.
基金This work was supported by the NationaNatural Science Foundation of China (No.30572096) andBeijing Natural Science Foundation (No.5052024).
文摘Objective： To investigate the role of Spl as transcription factor required for transactivation of LRP16 gene by estrogen. Methods： Specific antibodies of ERα and Spl were used to precipitate the target DNA/protein complexes of MCF-7 cells at different time points after estrogen treatment （Chromatin immunoprecipitation assay）, the promoter region of LRP16 gene was amplified by semi-nested polymerase chain reaction （snPCR）. Small interfering RNA （siRNA） against Spl was transiently cotransfected with LRP16-Luc （containing the region from -213bp to -126bp of LRP16 gene promoter）in MCF-7 cells. The luciferase activities were measured by dual-luciferase assay. Results： The results of chromatin immunoprecipitation assay showed that Spl protein directly bound to the -213bp to -126bp region of LRP16 gene, and ERα could enhance the affinity of Spl to DNA. Spl-siRNA specifically decreased the transactivation of LRP16-Luc by 1713-estradio1 to 70-80%. Conclusion： The estrogen-induced transactivation of the human LRP16 gene was mediated by Spl protein. Moreover, the interactions of ERα/Sp1 functional complex with LRP16 promoter DNA were required for enhanced LRP16 gene transactivation.
