AIM:To explore the effect of co-host non-coding RNA(ncRNA)MIR503HG/miR-503-5p on the angiogenesis of pterygium.METHODS:MIR503HG/miR-503-5p/fibroblast growth factor 2(FGF2)expression levels in pterygium tissues,control...AIM:To explore the effect of co-host non-coding RNA(ncRNA)MIR503HG/miR-503-5p on the angiogenesis of pterygium.METHODS:MIR503HG/miR-503-5p/fibroblast growth factor 2(FGF2)expression levels in pterygium tissues,control conjunctival tissues,and human pterygium fibroblasts(HPF)were examined by reverse transcription-polymerase chain reaction(qRT-PCR)and immunohistochemical methods.Effects of MIR503HG/miR-503-5p on low molecular weight FGF2(LWM FGF2),migration and angiogenesis of human retinal microvascular endothelial cells(HRMEC)were determined in an HPF and HRMEC co-culture model using Western blots,wound healing assay,Matrigel-based tube formation assay,and Transwell assay.RESULTS:MIR503HG/miR-503-5p/FGF2 pathway was actively increased in pterygium tissue and there was a negative correlation between the expression of the two ncRNAs.FGF2 expression level was positively correlated with MIR503HG and negatively correlated with miR-503-5p.Overexpressed MIR503HG/miR-503-5p did not affect the migration and angiogenesis of HRMECs cultured separately,but significantly affected migration and angiogenesis of HRMEC in HPF and HRMEC co-culture models.Western blotting revealed that MIR503HG/miR-503-5p overexpression significantly increased LMW FGF2 expression in HPF.CONCLUSION:MIR503HG/miR-503-5p inhibits HRMEC migration and angiogenic function by interfering with the interaction between HPF and endothelial cells via reducing LMW FGF2 in HPF.展开更多
Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of eff...Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of mi R-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined.Here, we found that mi R-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified mi R-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of mi R-503-3p in breast cancer cells inhibited expression of epithelialemesenchymal transition（EMT）-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their m RNA30 untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for mi R-503-3p in induction of breast cancer EMT and suggest that plasma mi R-503-3p may be a useful diagnostic biomarker for breast cancer.展开更多
基金Supported by the National Natural Science Foundation of China(No.81770898).
文摘AIM:To explore the effect of co-host non-coding RNA(ncRNA)MIR503HG/miR-503-5p on the angiogenesis of pterygium.METHODS:MIR503HG/miR-503-5p/fibroblast growth factor 2(FGF2)expression levels in pterygium tissues,control conjunctival tissues,and human pterygium fibroblasts(HPF)were examined by reverse transcription-polymerase chain reaction(qRT-PCR)and immunohistochemical methods.Effects of MIR503HG/miR-503-5p on low molecular weight FGF2(LWM FGF2),migration and angiogenesis of human retinal microvascular endothelial cells(HRMEC)were determined in an HPF and HRMEC co-culture model using Western blots,wound healing assay,Matrigel-based tube formation assay,and Transwell assay.RESULTS:MIR503HG/miR-503-5p/FGF2 pathway was actively increased in pterygium tissue and there was a negative correlation between the expression of the two ncRNAs.FGF2 expression level was positively correlated with MIR503HG and negatively correlated with miR-503-5p.Overexpressed MIR503HG/miR-503-5p did not affect the migration and angiogenesis of HRMECs cultured separately,but significantly affected migration and angiogenesis of HRMEC in HPF and HRMEC co-culture models.Western blotting revealed that MIR503HG/miR-503-5p overexpression significantly increased LMW FGF2 expression in HPF.CONCLUSION:MIR503HG/miR-503-5p inhibits HRMEC migration and angiogenic function by interfering with the interaction between HPF and endothelial cells via reducing LMW FGF2 in HPF.
基金supported by funding from the National Key Basic Research Program of China(973 Program,No.2012CB967003)the National Natural Science Foundation of China(Nos.81472661,21335007,and 81402463)the National High Technology Research and Development Program of China(863 Program,No.2015AA020104)
文摘Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of mi R-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined.Here, we found that mi R-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified mi R-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of mi R-503-3p in breast cancer cells inhibited expression of epithelialemesenchymal transition（EMT）-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their m RNA30 untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for mi R-503-3p in induction of breast cancer EMT and suggest that plasma mi R-503-3p may be a useful diagnostic biomarker for breast cancer.
