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| 1 | Nuclear Aurora kinase A switches m^(6)A reader YTHDC1 to enhance an oncogenic RNA splicing of tumor suppressor RBM4显示文摘Aberrant RNA splicing produces alternative isoforms of genes to facilitate tumor progression,yet how this process is regulated by oncogenic signal remains largely unknown.Here,we unveil that non-canonical activation of nuclear AURKA promotes an oncogenic RNA splicing of tumor suppressor RBM4 directed by m^(6)A reader YTHDC1 in lung cancer.Nuclear translocation of AURKA is a prerequisite for RNA aberrant splicing,specifically triggering RBM4 splicing from the full isoform(RBM4-FL)to the short isoform(RBM4-S)in a kinase-independent manner. | SiSi Li YangFan Qi JiaChuan Yu YuChao Hao Bin He MengJuan Zhang ZhenWei Dai TongHui Jiang SuYi Li Fang Huang Ning Chen Jing Wang MengYing Yang DaPeng Liang Fan An JinYao Zhao WenJun Fan YuJia Pan ZiQian Deng YuanYuan Luo Tao Guo Fei Peng ZhiJie Hou ChunLi Wang FeiMeng Zheng LingZhi Xu Jie Xu QingPing Wen BiLian Jin Yang Wang Quentin Liu | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 4 |
| 2 | Aberrant alternative splicing in breast cancer显示文摘Alternative splicing is critical for human gene expression regulation,which plays a determined role in expanding the diversity of functional proteins.Importantly,alternative splicing is a hallmark of cancer and a potential target for cancer therapeutics.Based on the statistical data,breast cancer is one of the top leading causes of cancer-related deaths in women worldwide.Strikingly,alternative splicing is closely associated with breast cancer development.Here,we seek to provide a general review of the relationship between alternative splicing and breast cancer.We introduce the process of alternative splicing and its regulatory role in cancers.In addition,we highlight the functions of aberrant alternative splicing and mutations of splicing factors in breast cancer progression.Moreover,we discuss the role of alternative splicing in cancer drug resistance and the potential of being targets for cancer therapeutics. | Quan Yang Jinyao Zhao Wenjing Zhang Dan Chen Yang Wang | 2019 | Journal of Molecular Cell Biology2019，11，10： | 3 |
| 3 | SRSF1 inhibits autophagy through regulating Bcl-x splicing and interacting with PIK3C3 in lung cancer显示文摘Alternative splicing is a critical process to generate protein diversity.However,whether and how alternative splicing regulates autophagy remains largely elusive.Here we systematically identify the splicing factor SRSF1 as an autophagy suppressor.Specifically,SRSF1 inhibits autophagosome formation by reducing the accumulation of LC3-ⅡI and numbers of autophagosomes in different cell lines.Mechanistically,SRSF1 promotes the splicing of the long isoform of Bcl-x that interacts with Beclinl,thereby dissociating the Beclin1-PIK3C3 complex.In addition,SRSF1 also directly interacts with PIK3C3 to disrupt the interaction between Beclinl and PIK3C3.Consequently,the decrease of SRSF1 stabilizes the Beclinl and PIK3C3 complex and activates autophagy.Interestingly,SRSF1 can be degraded by starvation-and oxidative stresses-induced autophagy through interacting with LC3-Ⅱ,whereas reduced SRSF1 further promotes autophagy.This positive feedback is critical to inhibiting Gefitinib-resistant cancer cell progression both in vitro and in vivo.Consistently,the expression level of SRSF1 is inversely correlated to LC3 level in clinical cancer samples.Our study not only provides mechanistic insights of alternative splicing in autophagy regulation but also discovers a new regulatory role of SRSF1 in tumorigenesis,thereby offering a novel avenue for potential cancer therapeutics. | Yuesheng Lv Wenjing Zhang Jinyao Zhao Bing Sun Yangfan Qi Haoyu Ji Chaoqun Chen Jinrui Zhang Junxiu Sheng Taishu Wang Daniel Dominguez Han Liu Quentin Liu Songshu Meng Xiaoling Li Yang Wang | 2021 | Signal Transduction and Targeted Therapy2021，6，4： | 2 |
| 4 | Astragalus polysaccharides enhance immune responses of HBV DNA vaccination via promoting the dendritic cell maturation and suppressing Treg frequency in mice显示文摘 | Xiaogang Du Bing Zhao Jinyao Li Xiaohan Cao Mingkun Diao Haibo Feng Xiaobing Chen Zhiyu Chen Xianyin Zeng | 2012 | International Immunopharmacology2012，，4： | 1 |
| 5 | Influence of hydroxylation and glyeosyla- tion in ring A of soybean isflavones on interaction with BSA 显示文摘 | Jinyao Zhao Fenglian Ren | 2009 | Spee- trochimica Acta Part A2009，，： | 1 |
| 6 | RBM4 dictates ESCC cell fate switch from cellular senescence to glutamine-addiction survival through inhibiting LKB1-AMPK-axis显示文摘Cellular senescence provides a protective barrier against tumorigenesis in precancerous or normal tissues upon distinct stressors.However,the detailed mechanisms by which tumor cells evade premature senescence to malignant progression remain largely elusive.Here we reported that RBM4 adversely impacted cellular senescence to favor glutamine-dependent survival of esophageal squamous cell carcinoma(ESCC)cells by dictating the activity of LKB1,a critical governor of cancer metabolism.The level of RBM4 was specifically elevated in ESCC compared to normal tissues,and RBM4 overexpression promoted the malignant phenotype.RBM4 contributed to overcome H-RAS-or doxorubicin-induced senescence,while its depletion caused P27-dependent senescence and proliferation arrest by activating LKB1-AMPK-mTOR cascade.Mechanistically,RBM4 competitively bound LKB1 to disrupt the LKB1/STRAD/MO25 heterotrimeric complex,subsequently recruiting the E3 ligase TRIM26 to LKB1,promoting LKB1 ubiquitination and degradation in nucleus.Therefore,such molecular process leads to bypassing senescence and sustaining cell proliferation through the activation of glutamine metabolism.Clinically,the ESCC patients with high RBM4 and low LKB1 have significantly worse overall survival than those with low RBM4 and high LKB1.The RBM4 high/LKB1 low expression confers increased sensitivity of ESCC cells to glutaminase inhibitor CB-839,providing a novel insight into mechanisms underlying the glutamine-dependency to improve the efficacy of glutamine inhibitors in ESCC therapeutics. | Lei Chen Wenjing Zhang Dan Chen Quan Yang Siwen Sun Zhenwei Dai Zhengzheng Li Xuemei Liang Chaoqun Chen Yuexia Jiao Lili Zhi Lianmei Zhao Jinrui Zhang Xuefeng Liu Jinyao Zhao Man Li Yang Wang Yangfan Qi | 2023 | Signal Transduction and Targeted Therapy2023，8，5： | 0 |
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