The published article titled“Swainsonine inhibits invasion and the EMT process in esophageal carcinoma cells by targeting twist1”has been retracted from Oncology Research,Vol.26,No.8,2018,pp.1207–1213.
Objective:Lung cancer is the most common cause of cancer-related deaths worldwide.Platinum-based chemotherapy is one of the main treatment options for patients with non-small cell lung cancer(NSCLC)but the effectivene...Objective:Lung cancer is the most common cause of cancer-related deaths worldwide.Platinum-based chemotherapy is one of the main treatment options for patients with non-small cell lung cancer(NSCLC)but the effectiveness of chemotherapy is encumbered by drug resistance.Therefore,understanding the molecular mechanisms underlying chemotherapy resistance is crucial in improving treatment outcomes and prognosis.Methods:The cell viability assay and apoptosis were used to analyze chemoresistance.Western blot analysis and wound healing testing were used to evaluate the epithelial-to-mesenchymal transition(EMT).Immunoprecipitation was used for analysis of protein modification.Promoter activity was determined using the luciferase reporter assay.Immunofluorescence staining was used to determine reactive oxygen species levels.The expression patterns of EMT markers and carnitine palmitoyltransferase 1C(CPT1C)were determined by Western blot analysis.Results:CPT1C,which was shown to be highly expressed in lung cancer,is associated with cisplatin resistance in NSCLC cells.CPT1C depletion increased NSCLC cell sensitivity to cisplatin,while overexpression of CPT1C increased NSCLC cell resistance to cisplatin.Induction of EMT mediated CPT1C-induced cisplatin resistance.Ectopic expression of Snail reversed the increase in cisplatin sensitivity triggered by CPT1C knockdown.Moreover,CPT1C was shown to be regulated at the post-translational level and an E3-ubiquitin ligase,NEDD4L,was shown to be a major regulator of CPT1C stability and activity.Conclusions:These data provide evidence for the first time that the lipid metabolism enzyme,CPT1C,mediates resistance to chemotherapy.Therefore,the use of combination therapy with a CPT1C inhibitor may be a promising new avenue in lung cancer treatment.展开更多
Background:Oral cancer remains a significant global health challenge,as it has high morbidity and mortality rates.Current treatments show limited efficacy and have severe side effects,prompting searches for new therap...Background:Oral cancer remains a significant global health challenge,as it has high morbidity and mortality rates.Current treatments show limited efficacy and have severe side effects,prompting searches for new therapeutic agents.SH003,a traditional herbal formulation comprising Astragalus membranaceus,Angelica gigas,and Trichosanthes kirilowii,has demonstrated potential anticancer properties in previous studies.However,its specific efficacy against oral cancer and the role of its key components,particularly Cucurbitacin D,remain underexplored.Methods:The cytotoxic effects of SH003 and its major components—i.e.,Cucurbitacin D,Decursin,Formononetin,and Nodakenin—were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide(MTT),Trypan Blue exclusion,and Lactate Dehydrogenase(LDH)release assays.Cell migration was analyzed via wound healing assays,and apoptosis induction was assessed using cell cycle analysis and caspase activation assays.Epithelial-tomesenchymal transition(EMT)marker expression(E-cadherin and N-cadherin)was measured using Western blotting and Quantitative reverse transcription PCR(qRT-PCR).Results:SH003 significantly reduced cell viability in a dosedependent manner,with YD-8 and YD-9 cells showing greater sensitivity than YD-38 cells.Of the individual compounds,Cucurbitacin D was identified as a key active agent,as it exhibited potent inhibition of cell migration and significant modulation of EMT markers,including the upregulation of E-cadherin and downregulation of N-cadherin.These effects were most pronounced in YD-9 cells.Conclusions:Taken together,these findings suggest that Cucurbitacin D plays a crucial role mediating the anticancer activity of SH003,particularly via the reversal of EMT and the reduction of migratory and invasive potential of oral cancer cells.This study provides valuable insight into the mechanistic basis of SH003,highlighting its potential as a therapeutic agent against oral cancer.Further research,including in vivo studies and clinical trials,is needed to elucidate its precise mechanisms and potential applications against other cancer types.展开更多
文摘The published article titled“Swainsonine inhibits invasion and the EMT process in esophageal carcinoma cells by targeting twist1”has been retracted from Oncology Research,Vol.26,No.8,2018,pp.1207–1213.
基金supported by the National Natural Science Foundation of China(Grant No.81872371)the Open Project Program of State Key Laboratory of Molecular Oncology(Grant No.SKL-KF-2019-11)+3 种基金the Program for Excellent Sci-tech Innovation Teams of Universities in Anhui Province(Grant No.2023AH010073)the Provincial-level Quality Project in Higher Education Institutions of Anhui Province(Grant No.2022jyxm1710)the College Students Innovation and Entrepreneurship Training Program(Grant No.S202310368028 and S202410368035)the Health Science Research Project of Anhui Province(Grant No.AHWJ2022a028)。
文摘Objective:Lung cancer is the most common cause of cancer-related deaths worldwide.Platinum-based chemotherapy is one of the main treatment options for patients with non-small cell lung cancer(NSCLC)but the effectiveness of chemotherapy is encumbered by drug resistance.Therefore,understanding the molecular mechanisms underlying chemotherapy resistance is crucial in improving treatment outcomes and prognosis.Methods:The cell viability assay and apoptosis were used to analyze chemoresistance.Western blot analysis and wound healing testing were used to evaluate the epithelial-to-mesenchymal transition(EMT).Immunoprecipitation was used for analysis of protein modification.Promoter activity was determined using the luciferase reporter assay.Immunofluorescence staining was used to determine reactive oxygen species levels.The expression patterns of EMT markers and carnitine palmitoyltransferase 1C(CPT1C)were determined by Western blot analysis.Results:CPT1C,which was shown to be highly expressed in lung cancer,is associated with cisplatin resistance in NSCLC cells.CPT1C depletion increased NSCLC cell sensitivity to cisplatin,while overexpression of CPT1C increased NSCLC cell resistance to cisplatin.Induction of EMT mediated CPT1C-induced cisplatin resistance.Ectopic expression of Snail reversed the increase in cisplatin sensitivity triggered by CPT1C knockdown.Moreover,CPT1C was shown to be regulated at the post-translational level and an E3-ubiquitin ligase,NEDD4L,was shown to be a major regulator of CPT1C stability and activity.Conclusions:These data provide evidence for the first time that the lipid metabolism enzyme,CPT1C,mediates resistance to chemotherapy.Therefore,the use of combination therapy with a CPT1C inhibitor may be a promising new avenue in lung cancer treatment.
基金supported by grants from the Seoul National University Bundang Hospital(SNUBH)Research Fund(Grant no.02-2020-0008)the Creative-Pioneering Researchers Program of Seoul National University(Grant no.860-20240109).
文摘Background:Oral cancer remains a significant global health challenge,as it has high morbidity and mortality rates.Current treatments show limited efficacy and have severe side effects,prompting searches for new therapeutic agents.SH003,a traditional herbal formulation comprising Astragalus membranaceus,Angelica gigas,and Trichosanthes kirilowii,has demonstrated potential anticancer properties in previous studies.However,its specific efficacy against oral cancer and the role of its key components,particularly Cucurbitacin D,remain underexplored.Methods:The cytotoxic effects of SH003 and its major components—i.e.,Cucurbitacin D,Decursin,Formononetin,and Nodakenin—were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide(MTT),Trypan Blue exclusion,and Lactate Dehydrogenase(LDH)release assays.Cell migration was analyzed via wound healing assays,and apoptosis induction was assessed using cell cycle analysis and caspase activation assays.Epithelial-tomesenchymal transition(EMT)marker expression(E-cadherin and N-cadherin)was measured using Western blotting and Quantitative reverse transcription PCR(qRT-PCR).Results:SH003 significantly reduced cell viability in a dosedependent manner,with YD-8 and YD-9 cells showing greater sensitivity than YD-38 cells.Of the individual compounds,Cucurbitacin D was identified as a key active agent,as it exhibited potent inhibition of cell migration and significant modulation of EMT markers,including the upregulation of E-cadherin and downregulation of N-cadherin.These effects were most pronounced in YD-9 cells.Conclusions:Taken together,these findings suggest that Cucurbitacin D plays a crucial role mediating the anticancer activity of SH003,particularly via the reversal of EMT and the reduction of migratory and invasive potential of oral cancer cells.This study provides valuable insight into the mechanistic basis of SH003,highlighting its potential as a therapeutic agent against oral cancer.Further research,including in vivo studies and clinical trials,is needed to elucidate its precise mechanisms and potential applications against other cancer types.
