The published article titled“MicroRNA-138 Inhibits Cell Growth,Invasion,and EMT of Non-Small Cell Lung Cancer via SOX4/p53 Feedback Loop”has been retracted fromOncology Research,Vol.26,No.3,2018,pp.385–400.DOI:10.3...The published article titled“MicroRNA-138 Inhibits Cell Growth,Invasion,and EMT of Non-Small Cell Lung Cancer via SOX4/p53 Feedback Loop”has been retracted fromOncology Research,Vol.26,No.3,2018,pp.385–400.DOI:10.3727/096504017X14973124850905 URL:https://www.techscience.com/or/v26n3/56651 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells.In addition,the western blots in this article were presented with atypical,unusually shaped and possibly anomalous protein bands in many cases.展开更多
Objectives:Cholecystokinin A receptor(CCKAR)has been linked to poor prognosis in colon cancer patients,but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive.This study ai...Objectives:Cholecystokinin A receptor(CCKAR)has been linked to poor prognosis in colon cancer patients,but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive.This study aimed to explore the effect of CCKAR on the invasive potential of colon cancer cells.Methods:Different human colon cancer cell lines were used.Gene expression was evaluated by reverse transcription polymerase chain reaction(RT-PCR)and quantitative real-time RT-PCR(qPCR),while protein expression and phosphorylation were assessed by Western blotting.Cell motility and invasiveness were examined through wound healing and invasion assays,respectively.Results:Our results showed that CCKAR expression levels varied across colon cancer cell lines,with DLD-1 and LoVo cells showing high expression.Knockdown of CCKAR significantly impaired the cell motility and invasiveness of DLD-1 and LoVo cells,downregulated integrinβ3 expression,and diminished the phosphorylation levels of focal adhesion kinase(FAK),Src,and paxillin.In addition,CCKAR knockdown modulated epithelialmesenchymal transition(EMT)markers ZO-1,E-cadherin,and vimentin and reduced urokinase-type plasminogen activator(uPA),uPA receptor(uPAR),Rho GTPase cell division control protein 42(CDC42)and RhoA,and matrix metalloproteinase-2(MMP-2).Conclusions:These findings indicate that CCKAR knockdown impairs the invasiveness of colon cancer cells,which may be attributed to modulating integrin/FAK/Rho GTPases,EMT markers,and the uPA/uPAR axis.It suggests that targeting CCKAR may represent a potential therapeutic strategy for colon cancer treatment.展开更多
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
文摘The published article titled“MicroRNA-138 Inhibits Cell Growth,Invasion,and EMT of Non-Small Cell Lung Cancer via SOX4/p53 Feedback Loop”has been retracted fromOncology Research,Vol.26,No.3,2018,pp.385–400.DOI:10.3727/096504017X14973124850905 URL:https://www.techscience.com/or/v26n3/56651 Following the publication,concerns have been raised about a number of figures in this article.An unexpected area of similarity was identified in terms of the cellular data,where the results from differently performed experiments were intended to have been shown,although the areas immediately surrounding this area featured comparatively different distributions of cells.In addition,the western blots in this article were presented with atypical,unusually shaped and possibly anomalous protein bands in many cases.
基金funded by Chung Shan Medical University Hospital(grant number CSH 2023-C-010)Buddhist Tzu Chi Medical Foundation,Dalin Tzu Chi Hospital(grant number DTCRD112(2)-I-24).
文摘Objectives:Cholecystokinin A receptor(CCKAR)has been linked to poor prognosis in colon cancer patients,but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive.This study aimed to explore the effect of CCKAR on the invasive potential of colon cancer cells.Methods:Different human colon cancer cell lines were used.Gene expression was evaluated by reverse transcription polymerase chain reaction(RT-PCR)and quantitative real-time RT-PCR(qPCR),while protein expression and phosphorylation were assessed by Western blotting.Cell motility and invasiveness were examined through wound healing and invasion assays,respectively.Results:Our results showed that CCKAR expression levels varied across colon cancer cell lines,with DLD-1 and LoVo cells showing high expression.Knockdown of CCKAR significantly impaired the cell motility and invasiveness of DLD-1 and LoVo cells,downregulated integrinβ3 expression,and diminished the phosphorylation levels of focal adhesion kinase(FAK),Src,and paxillin.In addition,CCKAR knockdown modulated epithelialmesenchymal transition(EMT)markers ZO-1,E-cadherin,and vimentin and reduced urokinase-type plasminogen activator(uPA),uPA receptor(uPAR),Rho GTPase cell division control protein 42(CDC42)and RhoA,and matrix metalloproteinase-2(MMP-2).Conclusions:These findings indicate that CCKAR knockdown impairs the invasiveness of colon cancer cells,which may be attributed to modulating integrin/FAK/Rho GTPases,EMT markers,and the uPA/uPAR axis.It suggests that targeting CCKAR may represent a potential therapeutic strategy for colon cancer treatment.
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.
