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您的检索式：作者名="Nengming Lin"
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| 1 | Deubiquitinase JOSD2 stabilizes YAP/TAZ to promote cholangiocarcinoma progression显示文摘Cholangiocarcinoma(CCA)has emerged as an intractable cancer with scanty therapeutic regimens.The aberrant activation of Yes-associated protein(YAP)and transcriptional co-activator with PDZ-binding motif(TAZ)are reported to be common in CCA patients.However,the underpinning mechanism remains poorly understood.Deubiquitinase(DUB)is regarded as a main orchestrator in maintaining protein homeostasis.Here,we identified Josephin domain-containing protein 2(JOSD2)as an essential DUB of YAP/TAZ that sustained the protein level through cleavage of polyubiquitin chains in a deubiquitinase activity-dependent manner.The depletion of JOSD2 promoted YAP/TAZ proteasomal degradation and significantly impeded CCA proliferation in vitro and in vivo.Further analysis has highlighted the positive correlation between JOSD2 and YAP abundance in CCA patient samples.Collectively,this study uncovers the regulatory effects of JOSD2 on YAP/TAZ protein stabilities and profiles its contribution in CCA malignant progression,which may provide a potential intervention target for YAP/TAZ-related CCA patients. | Meijia Qian Fangjie Yan Weihua Wang Jiamin Du Tao Yuan Ruilin Wu Chenxi Zhao Jiao Wang Jiabin Lu Bo Zhang Nengming Lin Xin Dong Xiaoyang Dai Xiaowu Dong Bo Yang Hong Zhu Qiaojun He | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 5 |
| 2 | DYRK1A suppression restrains Mcl-1 expression and sensitizes NSCLC cells to Bd-2 inhibitors显示文摘Objective:Mcl-1 overexpression confers acquired resistance to Bcl-2 inhibitors in non-small cell lung cancer(NSCLC),but no direct Mcl-1 inhibitor is currently available for clinical use.Thus,novel therapeutic strategies are urgently needed to target Mcl-1 and sensitize the anti-NSCLC activity of Bcl-2 inhibitors.Methods:Cell proliferation was measured using sulforhodamine B and colony formation assays,and apoptosis was detected with Annexin V-FITC staining.Gene expression was manipulated using siRNAs and plasmids.Real-time PCR and Western blot were used to measure mRNA and protein levels.Immunoprecipitation and immunofluorescence were used to analyze co-localization o f dual specificity tyrosine-phosphorylation-regulated kinase 1A(DYRK1A)and Mcl-1.Results:Suppression of DYRK1A resulted in reduced Mcl-1 expression in NSCLC cells,whereas overexpression of DYRK1A significantly increased Mcl-1 expression.Suppression of DYRK1A did not alter Mcl-1 mRNA levels,but did result in an accelerated degradation o f Mcl-1 protein in NSCLC cells.Furthermore,DYRK1A mediated proteasome-dependent degradation o f Mcl-1 in NSCLC cells,and DYRK1A co-localized with Mcl-1 in NSCLC cells and was co-expressed with Mcl-1 in tumor samples from lung cancer patients,suggesting that Mcl-1 may be a novel DYRK1A substrate.We showed that combined therapy with harmine and Bcl-2 antagonists significantly inhibited cell proliferation and induced apoptosis in NSCLC cell lines as well as primary NSCLC cells.Conclusions:Mcl-1 is a novel DYRK1A substrate,and the role of DYRK1A in promoting Mcl-1 stability makes it an attractive target for decreasing Bcl-2 inhibitor resistance. | Yangling Li Dongmei Zhou Shuang Xu Mingjun Rao Zuoyan Zhang Linwen Wu Chong Zhang Nengming Lin | 2020 | Cancer Biology & Medicine2020，17，2： | 2 |
| 3 | Erratum to DYRK1A suppression restrains Mcl-1 expression and sensitizes NSCLC cells to Bcl-2 inhibitors显示文摘In the published paper1,errors appeared in Figure 1D on page 391.In Figure 1D,an incorrect gel image was shown for Bcl-xL in NCI-H1299 cells.Figure 1D has been updated to correct the mistake above.The errors do not affect the conclusions of this article.We apologize for the errors and for any confusion that they may have caused. | Yangling Li Dongmei Zhou Shuang Xu Mingjun Rao Zuoyan Zhang Linwen Wu Chong Zhang Nengming Lin | 2022 | Cancer Biology & Medicine2022，19，7： | 0 |
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