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 ...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.展开更多
During oncogenesis,the hyper-activation of proto-oncogenes and defection of tumor suppressor genes（Zhao et al.,2012,2016a）can regulate cell proliferation,differentiation,apoptosis,and cell-to-cell communication（Bal...During oncogenesis,the hyper-activation of proto-oncogenes and defection of tumor suppressor genes（Zhao et al.,2012,2016a）can regulate cell proliferation,differentiation,apoptosis,and cell-to-cell communication（Balmain et al.,2003;Haber and Settleman,2007）.Recent evidence has shown that non-coding RNAs, such as microRNAs （miRNAs） （Chen, 2005）, and long non- coding RNAs （lncRNAs）, can also act as oncogenes to initiate and promote cancer progression.展开更多
Triple-negative breast cancer(TNBC)is the most malignant subtype of breast cancer that lacks reliable targets for diagnosis and therapy.Non-coding RNA(ncRNA)-encoded products hold promise for addressing this unmet nee...Triple-negative breast cancer(TNBC)is the most malignant subtype of breast cancer that lacks reliable targets for diagnosis and therapy.Non-coding RNA(ncRNA)-encoded products hold promise for addressing this unmet need.By analyzing the reported ribosomal RNA sequencing data,combined with the TCGA,ORFfinder,SmProt databases,we identified CDKN2B-AS1,a TNBC-upregulated lncRNA encoding a 66-amino-acid peptide via CUG-initiated translation.CRISPR-Cas9 gene editing and mass spectrometry confirmed endogenous expression of this peptide,designated 66CTG,in TNBC cells.Functionally independently of its host RNA,66CTG promoted the proliferation of TNBC cells and the tumor growth of TNBC xenograft by stabilizing c-Myc protein and enhancing Cyclin D1 transcription.Immunohistochemistry of 89 clinical TNBC paraffin samples revealed positive correlations among 66CTG,c-Myc,and Cyclin D1 expression levels.展开更多
Objective To explore the effects of liposome C erbB 2 antisense phosphorothioate oligodeoxynucleotides (S ODNs) on C erbB 2 proto oncogene expression and cell proliferation in human ovarian cancer cells Metho...Objective To explore the effects of liposome C erbB 2 antisense phosphorothioate oligodeoxynucleotides (S ODNs) on C erbB 2 proto oncogene expression and cell proliferation in human ovarian cancer cells Methods The effects of liposome C erbB 2 S ODNs on C erbB 2 protein expression, cell cycle and cell proliferation in human ovarian cancer cells were studied by means of flow cytometry and 3H thymidine incorporation Results Liposome C erbB 2 S ODNs can specifically reduce C erbB 2 protein expression in human ovarian cancer cells, accompanied by a 30% inhibition of cell proliferation The effectiveness of liposome C erbB 2 S ODNs on the expression of C erbB 2 was about 40 times higher than that of C erbB 2 S ODNs Conclusions The data suggest that antisense therapy might be a useful method of gene therapy in ovarian cancer The effectiveness of C erbB 2 S ODNs could be greatly increased by adsorption of S ODNs by liposomes展开更多
文摘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.
文摘During oncogenesis,the hyper-activation of proto-oncogenes and defection of tumor suppressor genes（Zhao et al.,2012,2016a）can regulate cell proliferation,differentiation,apoptosis,and cell-to-cell communication（Balmain et al.,2003;Haber and Settleman,2007）.Recent evidence has shown that non-coding RNAs, such as microRNAs （miRNAs） （Chen, 2005）, and long non- coding RNAs （lncRNAs）, can also act as oncogenes to initiate and promote cancer progression.
基金supported by National Key Research and Development Program of China(2023YFA1800500,2023ZD0502200,SQ2023AAA030478,2020YFA0112300)National Natural Science Foundation of China(82203413,U2102203,82430084,82173014,82472806)+5 种基金Biomedical Projects of Yunnan Key Science and Technology Program(202302AA310046)Yunnan Fundamental Research Projects(Major project:202501AS070023,202201BC070002,General project:202401AT070171,202201AT070290)Yunnan Academician Expert Workstation(202505AF350058)Yunnan Revitalization Talent Support Program(Yunling Shcolar)Yunnan Revitalization Talent Support Program,Joint Special Funds for the Department of Science and Technology of Yunnan Province-Kunming Medical University(202401AY070001-026)The Innovative Research Team of Yunnan Province(202405AS350016).
文摘Triple-negative breast cancer(TNBC)is the most malignant subtype of breast cancer that lacks reliable targets for diagnosis and therapy.Non-coding RNA(ncRNA)-encoded products hold promise for addressing this unmet need.By analyzing the reported ribosomal RNA sequencing data,combined with the TCGA,ORFfinder,SmProt databases,we identified CDKN2B-AS1,a TNBC-upregulated lncRNA encoding a 66-amino-acid peptide via CUG-initiated translation.CRISPR-Cas9 gene editing and mass spectrometry confirmed endogenous expression of this peptide,designated 66CTG,in TNBC cells.Functionally independently of its host RNA,66CTG promoted the proliferation of TNBC cells and the tumor growth of TNBC xenograft by stabilizing c-Myc protein and enhancing Cyclin D1 transcription.Immunohistochemistry of 89 clinical TNBC paraffin samples revealed positive correlations among 66CTG,c-Myc,and Cyclin D1 expression levels.
基金ThisworkwassupportedbytheNationalNaturalScienceFoundationof China (No 39470 72 4)
文摘Objective To explore the effects of liposome C erbB 2 antisense phosphorothioate oligodeoxynucleotides (S ODNs) on C erbB 2 proto oncogene expression and cell proliferation in human ovarian cancer cells Methods The effects of liposome C erbB 2 S ODNs on C erbB 2 protein expression, cell cycle and cell proliferation in human ovarian cancer cells were studied by means of flow cytometry and 3H thymidine incorporation Results Liposome C erbB 2 S ODNs can specifically reduce C erbB 2 protein expression in human ovarian cancer cells, accompanied by a 30% inhibition of cell proliferation The effectiveness of liposome C erbB 2 S ODNs on the expression of C erbB 2 was about 40 times higher than that of C erbB 2 S ODNs Conclusions The data suggest that antisense therapy might be a useful method of gene therapy in ovarian cancer The effectiveness of C erbB 2 S ODNs could be greatly increased by adsorption of S ODNs by liposomes
