In the article“Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene”(Oncology Research.2024,Vol.32,No.7,pp.1185–1195.doi:10....In the article“Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene”(Oncology Research.2024,Vol.32,No.7,pp.1185–1195.doi:10.32604/or.2023.030771,https://www.techscience.com/or/v32n7/57163),an inadvertent error occurred during the compilation of Fig.3H.This needed corrections to ensure the accuracy and integrity of the data presented.展开更多
As living conditions improve and diagnostic capabilities advance,the incidence of tumors has increased,with cancer becoming a leading cause of death worldwide.Surgery,chemotherapy,and radiotherapy are the most common ...As living conditions improve and diagnostic capabilities advance,the incidence of tumors has increased,with cancer becoming a leading cause of death worldwide.Surgery,chemotherapy,and radiotherapy are the most common treatments.Despite advances in treatment options,chemotherapy remains a routine first-line treatment for most tumors.Due to the continuous and extensive use of chemotherapy drugs,tumor resistance often develops,becoming a significant cause of treatment failure and poor prognosis.Recent research has increasingly focused on how long stranded noncoding RNAs(LncRNAs)influence the development of malignant tumors and drug resistance by regulating gene expression and other biological mechanisms during cell growth.Studies have demonstrated that variations in lncRNA expression levels,influenced by both interpatient variability and intratumoral genetic and epigenetic differences,are closely linked to tumor drug resistance.Therefore,this review advocates using lncRNA as a framework to investigate the regulation of genes associated with drug resistance,proposing lncRNA-targeted therapeutic strategies to potentially increase the efficacy of chemotherapy,improve patient outcomes,and guide future research directions.展开更多
In the current era of molecular biology,where the major components of transcription,translation,and chromatin regulation have been extensively described,identifying fine regulators that confer spatial and temporal spe...In the current era of molecular biology,where the major components of transcription,translation,and chromatin regulation have been extensively described,identifying fine regulators that confer spatial and temporal specificity to gene expression becomes increasingly necessary.Among the most intriguing of these are long non-coding RNAs(lncRNAs).Once defined by their lack of coding potential and considered as transcriptional noise,lncRNAs have been,for the last decades,emerging as critical regulators with unique structural and functional versatility:they can fold into complex conformations or scaffold protein complexes,interact with DNA or other RNAs,guide chromatin remodelers,or act as molecular decoys.As such,they are increasingly recognized not merely as byproducts of transcription but as central players in gene regulation(Yang et al.,2023).展开更多
Endochondral bone formation is an important route for bone repair.Although emerging evidence has revealed the functions of long non-coding RNAs(lncRNAs)in bone and cartilage development,the effect of lncRNAs in endoch...Endochondral bone formation is an important route for bone repair.Although emerging evidence has revealed the functions of long non-coding RNAs(lncRNAs)in bone and cartilage development,the effect of lncRNAs in endochondral bone repair is still largely unknown.Here,we identified a lncRNA,named Hypertrophic Chondrocyte Angiogenesis-related lncRNA(HCAR),and proved it to promote the endochondral bone repair by upregulating the expression of matrix metallopeptidase 13(Mmp13)and vascular endothelial growth factorα(Vegfa)in hypertrophic chondrocytes.Lnc-HCAR knockdown in hypertrophic chondrocytes restrained the cartilage matrix remodeling and decrease the CD31hiEmcnhi vessels number in a bone repair model.Mechanistically,we proved that lnc-HCAR was mainly enriched in the cytoplasm using fluorescence in situ hybridization(FISH)assay,and it acted as a molecular sponge for miR-15b-5p.Further,in hypertrophic chondrocytes,lnc-HCAR competitively bound to miR-15b-5p to increase Vegfa and Mmp13 expression.Our results proved that lncRNA is deeply involved in endochondral bone repair,which will provide a new theoretical basis for future strategies for promoting fracture healing.展开更多
Metabolic dysfunction-associated steatotic liver disease(MASLD),previously referred to as non-alcoholic fatty liver disease,encompasses a broad range of hepatic metabolic disorders primarily characterised by the disru...Metabolic dysfunction-associated steatotic liver disease(MASLD),previously referred to as non-alcoholic fatty liver disease,encompasses a broad range of hepatic metabolic disorders primarily characterised by the disruption of hepatic lipid metabolism,hepatic lipid accumulation and steatosis.Severe cases of MASLD might progress to metabolic dysfunction-associated steatohepatitis,characterised by hepatic inflammation,hepatocyte ballooning degeneration,activation of hepatic stellate cells(HSCs)and fibrogenesis.It may further progress to hepatocellular carcinoma.In the liver,long non-coding RNAs(lncRNAs)target multiple metabolic pathways in hepatocytes,HSCs,and Kupffer cells at different stages of MASLD and liver fibrosis.In this study,we overview recent findings on the potential role of lncRNAs in the pathogenesis of MASLD and liver fibrosis via modulation of de novo lipid synthesis,fatty acidβ-oxidation,lipotoxicity,oxidative stress,metabolic inflammation,mammalian target of rapamycin signalling,apoptosis,ubiquitination and fibrogenesis.We critically assess the literature reports that investigate the complex interplay between lncRNA,microRNA and key mediators in liver injury,in both human participants and animal models of MASLD and liver fibrosis.We also highlight the therapeutic potential of lncRNAs in chronic liver diseases.展开更多
文摘In the article“Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene”(Oncology Research.2024,Vol.32,No.7,pp.1185–1195.doi:10.32604/or.2023.030771,https://www.techscience.com/or/v32n7/57163),an inadvertent error occurred during the compilation of Fig.3H.This needed corrections to ensure the accuracy and integrity of the data presented.
基金supported by the grant of the Medicine and Health Care Science and Technology Development Plan Projects Foundation of Shandong Province(No.202301060260).
文摘As living conditions improve and diagnostic capabilities advance,the incidence of tumors has increased,with cancer becoming a leading cause of death worldwide.Surgery,chemotherapy,and radiotherapy are the most common treatments.Despite advances in treatment options,chemotherapy remains a routine first-line treatment for most tumors.Due to the continuous and extensive use of chemotherapy drugs,tumor resistance often develops,becoming a significant cause of treatment failure and poor prognosis.Recent research has increasingly focused on how long stranded noncoding RNAs(LncRNAs)influence the development of malignant tumors and drug resistance by regulating gene expression and other biological mechanisms during cell growth.Studies have demonstrated that variations in lncRNA expression levels,influenced by both interpatient variability and intratumoral genetic and epigenetic differences,are closely linked to tumor drug resistance.Therefore,this review advocates using lncRNA as a framework to investigate the regulation of genes associated with drug resistance,proposing lncRNA-targeted therapeutic strategies to potentially increase the efficacy of chemotherapy,improve patient outcomes,and guide future research directions.
基金the support of Saclay Plant Sciences(SPS,ANR-17-EUR-0007)supported by the RIBORES grant from the French Agence Nationale pour la Recherche(ANR-22-CE92-0018).
文摘In the current era of molecular biology,where the major components of transcription,translation,and chromatin regulation have been extensively described,identifying fine regulators that confer spatial and temporal specificity to gene expression becomes increasingly necessary.Among the most intriguing of these are long non-coding RNAs(lncRNAs).Once defined by their lack of coding potential and considered as transcriptional noise,lncRNAs have been,for the last decades,emerging as critical regulators with unique structural and functional versatility:they can fold into complex conformations or scaffold protein complexes,interact with DNA or other RNAs,guide chromatin remodelers,or act as molecular decoys.As such,they are increasingly recognized not merely as byproducts of transcription but as central players in gene regulation(Yang et al.,2023).
基金This work was supported by Key Program of Natural Science Foundation of China(No.81930067)General Program of Nature Science Foundation of China(No.31870962)+2 种基金the Key Project of Logistics Research Plan of the PLA(No.AWS17J004-02-06)the Medical Science and Technology Youth Cultivation Project of PLA(No.20QNPY022)Medical innovation capability upgrading Plan of Southwest Hospital(No.SWH2018LJ-03).
文摘Endochondral bone formation is an important route for bone repair.Although emerging evidence has revealed the functions of long non-coding RNAs(lncRNAs)in bone and cartilage development,the effect of lncRNAs in endochondral bone repair is still largely unknown.Here,we identified a lncRNA,named Hypertrophic Chondrocyte Angiogenesis-related lncRNA(HCAR),and proved it to promote the endochondral bone repair by upregulating the expression of matrix metallopeptidase 13(Mmp13)and vascular endothelial growth factorα(Vegfa)in hypertrophic chondrocytes.Lnc-HCAR knockdown in hypertrophic chondrocytes restrained the cartilage matrix remodeling and decrease the CD31hiEmcnhi vessels number in a bone repair model.Mechanistically,we proved that lnc-HCAR was mainly enriched in the cytoplasm using fluorescence in situ hybridization(FISH)assay,and it acted as a molecular sponge for miR-15b-5p.Further,in hypertrophic chondrocytes,lnc-HCAR competitively bound to miR-15b-5p to increase Vegfa and Mmp13 expression.Our results proved that lncRNA is deeply involved in endochondral bone repair,which will provide a new theoretical basis for future strategies for promoting fracture healing.
基金supported by the British Heart Foundation(UK)(PG/19/86/34788)Northern Ireland Chest,Heart and Stroke Association(UK)(2019_08).
文摘Metabolic dysfunction-associated steatotic liver disease(MASLD),previously referred to as non-alcoholic fatty liver disease,encompasses a broad range of hepatic metabolic disorders primarily characterised by the disruption of hepatic lipid metabolism,hepatic lipid accumulation and steatosis.Severe cases of MASLD might progress to metabolic dysfunction-associated steatohepatitis,characterised by hepatic inflammation,hepatocyte ballooning degeneration,activation of hepatic stellate cells(HSCs)and fibrogenesis.It may further progress to hepatocellular carcinoma.In the liver,long non-coding RNAs(lncRNAs)target multiple metabolic pathways in hepatocytes,HSCs,and Kupffer cells at different stages of MASLD and liver fibrosis.In this study,we overview recent findings on the potential role of lncRNAs in the pathogenesis of MASLD and liver fibrosis via modulation of de novo lipid synthesis,fatty acidβ-oxidation,lipotoxicity,oxidative stress,metabolic inflammation,mammalian target of rapamycin signalling,apoptosis,ubiquitination and fibrogenesis.We critically assess the literature reports that investigate the complex interplay between lncRNA,microRNA and key mediators in liver injury,in both human participants and animal models of MASLD and liver fibrosis.We also highlight the therapeutic potential of lncRNAs in chronic liver diseases.
