At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),who...At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),whose high expression not only aggravates ovarian cancer but also can induce tumorigenesis and endometrial cancer progression,has not been studied in CC.The objective of this study was to investigate the expression and the underlying role of PCGEM1 in CC.The relative expression of PCGEM1 in CC cells was detected by real-time PCR.After the suppression of PCGEM1 expression by shRNA,the changes in the proliferation,migration,and invasion capacities were detected via CCK-8 assay,EdU assay,and colony formation assay wound healing assay.Transwell assay and the changes in expressions of epithelial-to-mesenchymal transition(EMT)markers were determined by western blot and immunofluorescence.The interplay among PCGEM1,miR-642a-5p,and kinesin family member 5B(KIF5B)was confirmed by bioinformatics analyses and luciferase reporter assay.Results showed that PCGEM1 expressions were up-regulated within CC cells.Cell viabilities,migration,and invasion were remarkably reduced after the suppression of PCGEM1 expression by shRNA in Hela and SiHa cells.N-cadherin was silenced,but E-cadherin expression was elevated by sh-PCGEM1.Moreover,by sponging miR-642a-5p in CC,PCGEM1 was verified as a competitive endogenous RNA(ceRNA)that modulates KIF5B levels.MiR-642a-5p down-regulation partially rescued sh-PCGEM1’s inhibitory effects on cell proliferation,migration,invasion,and EMT process.In conclusion,the PCGEM1/miR-642a-5p/KIF5B signaling axis might be a novel therapeutic target in CC.This study provides a research basis and new direction for targeted therapy of CC.展开更多
BACKGROUND MET fusion is a key driver mutation,but it is rare in gastric cancer(GC).Several MET(hepatocyte growth factor receptor)inhibitors have been approved for the treatment of MET-positive patients,but the tumor ...BACKGROUND MET fusion is a key driver mutation,but it is rare in gastric cancer(GC).Several MET(hepatocyte growth factor receptor)inhibitors have been approved for the treatment of MET-positive patients,but the tumor response is heterogeneous.With the development of next-generation sequencing,diverse MET fusion partner genes have been identified.We herein report a fusion variant involving KIF5BMET in GC.CASE SUMMARY After thoracoscopic inferior lobectomy plus lymph node dissection under general anesthesia,a“tumor within a tumor”was found in the lung tumor tissue of a 64-year-old non-smoking male patient.Combining the medical history and the results of enzyme labeling,the focal area was considered to be GC.To seek potential therapeutic regimens,an intergenic region between KIF5B and MET fusion was identified.This fusion contains a MET kinase domain and coil-coiled domains encoded by KIF5B exons 1-25,which might drive the oncogenesis.CONCLUSION Our finding could extend the spectrum and genomic landscape of MET fusions in GC and favor the development of personalized therapy.展开更多
基金the Nantong Municipal Health Commission Research Project(MB2021054)for this study.
文摘At present,the role of many long non-coding RNAs(lncRNAs)as tumor suppressors in the formation and development of cervical cancer(CC)has been studied.However,lncRNA prostate cancer gene expression marker 1(PCGEM1),whose high expression not only aggravates ovarian cancer but also can induce tumorigenesis and endometrial cancer progression,has not been studied in CC.The objective of this study was to investigate the expression and the underlying role of PCGEM1 in CC.The relative expression of PCGEM1 in CC cells was detected by real-time PCR.After the suppression of PCGEM1 expression by shRNA,the changes in the proliferation,migration,and invasion capacities were detected via CCK-8 assay,EdU assay,and colony formation assay wound healing assay.Transwell assay and the changes in expressions of epithelial-to-mesenchymal transition(EMT)markers were determined by western blot and immunofluorescence.The interplay among PCGEM1,miR-642a-5p,and kinesin family member 5B(KIF5B)was confirmed by bioinformatics analyses and luciferase reporter assay.Results showed that PCGEM1 expressions were up-regulated within CC cells.Cell viabilities,migration,and invasion were remarkably reduced after the suppression of PCGEM1 expression by shRNA in Hela and SiHa cells.N-cadherin was silenced,but E-cadherin expression was elevated by sh-PCGEM1.Moreover,by sponging miR-642a-5p in CC,PCGEM1 was verified as a competitive endogenous RNA(ceRNA)that modulates KIF5B levels.MiR-642a-5p down-regulation partially rescued sh-PCGEM1’s inhibitory effects on cell proliferation,migration,invasion,and EMT process.In conclusion,the PCGEM1/miR-642a-5p/KIF5B signaling axis might be a novel therapeutic target in CC.This study provides a research basis and new direction for targeted therapy of CC.
文摘BACKGROUND MET fusion is a key driver mutation,but it is rare in gastric cancer(GC).Several MET(hepatocyte growth factor receptor)inhibitors have been approved for the treatment of MET-positive patients,but the tumor response is heterogeneous.With the development of next-generation sequencing,diverse MET fusion partner genes have been identified.We herein report a fusion variant involving KIF5BMET in GC.CASE SUMMARY After thoracoscopic inferior lobectomy plus lymph node dissection under general anesthesia,a“tumor within a tumor”was found in the lung tumor tissue of a 64-year-old non-smoking male patient.Combining the medical history and the results of enzyme labeling,the focal area was considered to be GC.To seek potential therapeutic regimens,an intergenic region between KIF5B and MET fusion was identified.This fusion contains a MET kinase domain and coil-coiled domains encoded by KIF5B exons 1-25,which might drive the oncogenesis.CONCLUSION Our finding could extend the spectrum and genomic landscape of MET fusions in GC and favor the development of personalized therapy.