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| 1 | Small-molecule inhibitor LF3 restrains the development of pulmonary hypertension through the Wnt/β-catenin pathway显示文摘Pulmonary hypertension(PH)associated with congenital heart disease is a progressive hemodynamic disease that can lead to increased pulmonary vascular resistance,vascular remodeling,and even right heart failure and death.LF3 is a novel inhibitor of the reporter gene activity ofβ-catenin/TCF4 interaction in the Wnt/β-catenin signal pathway.However,whether this action of LF3 can prevent PH development remains unclear.In this study,we investigated the therapeutic effect of LF3 in rat primary pulmonary artery smooth muscle cells(PASMCs)of the PH model.We found that LF3 inhibited the decrease in pulmonary artery acceleration time and ejection time by ultra-high-resolution ultrasound imaging and blocked the increase of pulmonary artery systolic pressure by using the BL420 biological function experimental system and right ventricular hypertrophy index by the electronic scales.Simultaneously,it prevented the increase ofα-smooth muscle actin and fibronectin and the decrease of elastin in pulmonary arteries of rats in the PH group,as revealed by an immunohistochemical analysis.Moreover,cell proliferation and migration assays showed that LF3 significantly reduced the proliferation and migration of PASMCs.Western blotting and quantitative real-time polymerase chain reaction analyses revealed that LF3 suppressed the expression of proliferating cell nuclear antigens and Bcl-2 and increased the expression of Bax but did not alter the expressions ofβ-catenin and TCF4.Taken together,LF3 can reduce the migration and proliferation of PASMCs and induce their apoptosis to prevent the development of PH.It would be worthwhile to explore the potential use of LF3 in the treatment of PH. | Yong Lei Qi Yang Yongmei Nie Juyi Wan Mingbin Deng | 2021 | Acta Biochimica et Biophysica Sinica2021，53，10： | 2 |
| 2 | Y-box protein-1 modulates circSPECC1 to promote glioma tumorigenesis via miR-615-5p/HIP1/AKT axis显示文摘Y-box binding protein-1(YB-1)is upregulated in glioma and plays an important role in its occurrence and drug resistance.However,the involved regulatory processes and downstream pathways are still unclear.Since various circular RNAs(circRNAs)and microRNAs(miRNAs)also play roles in the pathogenesis of glioma,we hypothesize that YB-1 may exert its function through a circRNA-miRNA-protein interaction network.In this study,we use the RNA binding protein immunoprecipitation assay and quantitative reverse transcription polymerase chain reaction to determine the circRNAs involved in the regulation of YB-1 and further elucidate their biological functions.The level of circSPECC1(hsa_circ_0000745)modulated by YB-1 is significantly upregulated in the U251 and U87 glioma cell lines.Downregulation of circSPECC1 markedly inhibits the proliferation and invasiveness of U251 and U87 cells by inducing apoptosis.Bioinformatics analysis reveals that miR-615-5p could interact with circSPECC1 and huntingtin-interacting protein-1(HIP-1).Then we determine the interactions between miR-615-5p,circSPECC1,and HIP1 using dual luciferase reporter system and pull-down assays.Mechanistic analysis indicates that the downregulation of circSPECC1 results in a decreased HIP1 expression.This study demonstrates that circSPECC1 modulated by YB-1 is increased in glioma cell lines.In addition,circSPECC1 promotes glioma growth through the upregulation of HIP1 by sponging miR-615-5p and targeting the HIP1/AKT pathway.This indicates that YB-1 and circSPECC1 may both be promising targets for glioma treatment. | Ping Lan Meihe Li Ying Wang Jingwen Wang Luyao Li Sha Zhang Xuan Zhang Caihong Ran Jin Zheng Huilin Gong | 2023 | Acta Biochimica et Biophysica Sinica2023，55，12： | 0 |
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