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| 1 | AXL is a candidate receptor for SARS-CoV-2 that promotes infection of pulmonary and bronchial epithelial cells显示文摘The current coronavirus disease 2019(COVID-19)pandemic presents a global public health challenge.The viral pathogen responsible,severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),binds to the host receptor ACE2 through its spike(S)glycoprotein,which mediates membrane fusion and viral entry.Although the role of ACE2 as a receptor for SARS-CoV-2 is clear,studies have shown that ACE2 expression is extremely low in various human tissues,especially in the respiratory tract.Thus,other host receptors and/or co-receptors that promote the entry of SARS-CoV-2 into cells of the respiratory system may exist.In this study,we found that the tyrosine-protein kinase receptor UFO(AXL)specifically interacts with the N-terminal domain of SARS-CoV-2 S.Using both a SARS-CoV-2 virus pseudotype and authentic SARS-CoV-2,we found that overexpression of AXL in HEK293T cells promotes SARS-CoV-2 entry as efficiently as overexpression of ACE2,while knocking out AXL significantly reduces SARS-CoV-2 infection in HI 299 pulmonary cells and in human primary lung epithelial cells.Soluble human recombinant AXL blocks SARS-CoV-2 infection in cells expressing high levels of AXL.The AXL expression level is well correlated with SARS-CoV-2 S level in bronchoalveolar lavage fluid cells from COVID-19 patients.Taken together,our findings suggest that AXL is a novel candidate receptor for SARS-CoV-2 which may play an important role in promoting viral infection of the human respiratory system and indicate that it is a potential target for future clinical intervention strategies. | Shuai Wang Zongyang Qiu Yingnan Hou Xiya Deng Wei Xu Tingting Zheng Peihan Wu Shaofang Xie Weixiang Bian Chong Zhang Zewei Sun Kunpeng Liu Chao Shan Aifu Lin Shibo Jiang Youhua Xie Qiang Zhou Lu Lu Jing Huang Xu Li | 2021 | Cell Research2021，31，2： | 39 |
| 2 | A phosphatidic acid-binding lncRNA SNHG9 facilitates LATS1 liquid–liquid phase separation to promote oncogenic YAP signaling显示文摘Long noncoding RNAs(lncRNAs)are emerging as a new class of important regulators of signal transduction in tissue homeostasis and cancer development.Liquid–liquid phase separation(LLPS)occurs in a wide range of biological processes,while its role in signal transduction remains largely undeciphered.In this study,we uncovered a lipid-associated lncRNA,small nucleolar RNA host gene 9(SNHG9)as a tumor-promoting lncRNA driving liquid droplet formation of Large Tumor Suppressor Kinase 1(LATS1)and inhibiting the Hippo pathway.Mechanistically,SNHG9 and its associated phosphatidic acids(PA)interact with the C-terminal domain of LATS1,promoting LATS1 phase separation and inhibiting LATS1-mediated YAP phosphorylation.Loss of SNHG9 suppresses xenograft breast tumor growth.Clinically,expression of SNHG9 positively correlates with YAP activity and breast cancer progression.Taken together,our results uncover a novel regulatory role of a tumor-promoting lncRNA(i.e.,SNHG9)in signal transduction and cancer development by facilitating the LLPS of a signaling kinase(i.e.,LATS1). | Rui-Hua Li Tian Tian Qi-Wei Ge Xin-Yu He Cheng-Yu Shi Jun-Hong Li Zhen Zhang Fang-Zhou Liu Ling-Jie Sang Zuo-Zhen Yang Ya-Zhuo Liu Yan Xiong Qingfeng Yan Xu Li Huai-Qiang Ju Jian Liu Liang-Jing Wang Jian-Zhong Shao Wenqi Wang Tianhua Zhou Aifu Lin | 2021 | Cell Research2021，31，10： | 6 |
| 3 | Tumor immune checkpoints and their associated inhibitors显示文摘Immunological evasion is one of the defining characteristics of cancers,as the immune modification of an immune checkpoint(IC)confers immune evasion capabilities to tumor cells.Multiple ICs,such as programmed cell death protein-1(PD-1)and cytotoxic T-lymphocyte-associated antigen-4(CTLA-4),can bind to their respective receptors and reduce tumor immunity in a variety of ways,including blocking immune cell activation signals.IC blockade(ICB)therapies targeting these checkpoint molecules have demonstrated significant clinical benefits.This is because antibody-based IC inhibitors and a variety of specific small molecule inhibitors can inhibit key oncogenic signaling pathways and induce durable tumor remission in patients with a variety of cancers.Deciphering the roles and regulatory mechanisms of these IC molecules will provide crucial theoretical guidance for clinical treatment.In this review,we summarize the current knowledge on the functional and regulatory mechanisms of these IC molecules at multiple levels,including epigenetic regulation,transcriptional regulation,and post-translational modifications.In addition,we provide a summary of the medications targeting various nodes in the regulatory pathway,and highlight the potential of newly identified IC molecules,focusing on their potential implications for cancer diagnostics and immunotherapy. | Zerui GAO Xingyi LING Chengyu SHI Ying WANG Aifu LIN | 2022 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2022，23，10： | 4 |
| 4 | Iron metabolism,ferroptosis,and lncRNA in cancer: knowns and unknowns显示文摘Cancer cells undergo substantial metabolic alterations to sustain increased energy supply and uncontrolled proliferation.As an essential trace element,iron is vital for many biological processes.Evidence has revealed that cancer cells deploy various mechanisms to elevate the cellular iron concentration to accelerate proliferation.Ferroptosis,a form of cell death caused by iron-catalyzed excessive peroxidation of polyunsaturated fatty acids(PUFAs),is a promising therapeutic target for therapyresistant cancers.Previous studies have reported that long noncoding RNA(lncRNA)is a group of critical regulators involved in modulating cell metabolism,proliferation,apoptosis,and ferroptosis.In this review,we summarize the associations among iron metabolism,ferroptosis,and ferroptosis-related lncRNA in tumorigenesis.This information will help deepen understanding of the role of lncRNA in iron metabolism and raise the possibility of targeting lncRNA and ferroptosis in cancer combination therapy. | Lei QU Xinyu HE Qian TANG Xiao FAN Jian LIU Aifu LIN | 2022 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2022，23，10： | 3 |
| 5 | YB1 regulates miR-205/200b-ZEB1 axis by inhibiting microRNA maturation in hepatocellular carcinoma显示文摘Background:Y-box binding protein 1(YB1 or YBX1)plays a critical role in tumorigenesis and cancer progression.However,whether YB1 affects malignant transformation by modulating non-codingRNAs remains largely unknown.This study aimed to investigate the relationship between YB1 and microRNAs and reveal the underlying mechanism by which YB1 impacts on tumor malignancy via miRNAs-mediated regulatory network.Methods:The biological functions of YB1 in hepatocellular carcinoma(HCC)cells were investigated by cell proliferation,wound healing,and transwell invasion assays.The miRNAs dysregulated by YB1 were screened by microarray analysis in HCC cell lines.The regulation of YB1 on miR-205 and miR-200b was determined by quantitative real-time PCR,dual-luciferase reporter assay,RNA immunoprecipitation,and pull-down assay.The relationships of YB1,DGCR8,Dicer,TUT4,and TUT1 were identified by pull-down and coimmunoprecipitation experiments.The cellular co-localization of YB1,DGCR8,and Dicer were detected by immunofluorescent staining.The in vivo effect of YB1 on tumor metastasis was determined by injecting MHCC97H cells transduced with YB1 shRNA or shControl via the tail vein in nude BALB/c mice.The expression levels of epithelial tomesenchymal transition markerswere detected by immunoblotting and immunohistochemistry assays.Results:YB1 promoted HCC cell migration and tumor metastasis by regulating miR-205/200b‒ZEB1 axis partially in a Snail-independent manner.YB1 suppressedmiR-205 and miR-200b maturation by interacting with the microprocessors DGCR8 and Dicer as well as TUT4 and TUT1 via the conserved cold shock domain.Subsequently,the downregulation of miR-205 and miR-200b enhanced ZEB1 expression,thus leading to increased cell migration and invasion.Furthermore,statistical analyses on gene expression data from HCC and normal liver tissues showed that YB1 expression was positively associated with ZEB1 expression and remarkably correlated with clinical prognosis.Conclusion:This study reveals a previously undescribed mechanism by which YB1 promotes cancer progression by regulating the miR-205/200b‒ZEB1 axis in HCC cells.Furthermore,these results highlight that YB1 may play biological functions via miRNAs-mediated gene regulation,and it can serve as a potential therapeutic target in human cancers. | Xiumei Liu Di Chen Huan Chen Wen Wang Yu Liu Yawei Wang Chao Duan Zhen Ning Xin Guo Wuxiyar Otkur Jing Liu Huan Qi Xiaolong Liu Aifu Lin Tian Xia Hong-xu Liu Hai-long Piao | 2021 | Cancer Communications2021，41，7： | 1 |
| 6 | Cancer immunotherapy: an evolving paradigm显示文摘The inhibition of the host’s natural immune response by tumor cells was widely reported in the early phases of the development of oncology therapy,and the concept of employing the host’s immune system to treat cancer,i.e.tumor immunotherapy,is not new.However,as a result of early theoretical constraints,clinical application of immunotherapy did not go smoothly and lagged significantly behind radiation and chemotherapy.The path has been winding,but the future now seems promising.Immunotherapy research has advanced enormously as a result of the maturing of immuno-editing theory and the creation of numerous technologies,despite a number of unsuccessful endeavors and clinical studies.Since around 1998,the US Food and Drug Administration(FDA)has approved a variety of tumor immunotherapies,including cytokines(interleukin-2,interferons),cancer vaccines(Provenge),immune checkpoint inhibitors(ipilimumab),and cellular therapies(chimeric antigen receptor-T(CAR-T)),signaling a boom in the field. | Aifu LIN | 2022 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2022，23，10： | 0 |
| 7 | LncFASA promotes cancer ferroptosis via modulating PRDX1 phase separation显示文摘Ferroptosis, a unique type of non-apoptotic cell death resulting from iron-dependent lipid peroxidation, has a potential physiological function in tumor suppression, but its underlying mechanisms have not been fully elucidated. Here, we report that the long non-coding RNA(lncRNA) LncFASA increases the susceptibility of triple-negative breast cancer(TNBC) to ferroptosis. As a tumor suppressor, LncFASA drives the formation of droplets containing peroxiredoxin1(PRDX1), a member of the peroxidase family, resulting in the accumulation of lipid peroxidation via the SLC7A11-GPX4 axis. Mechanistically, LncFASA directly binds to the Ahpc-TSA domain of PRDX1, inhibiting its peroxidase activity by driving liquid-liquid phase separation, which disrupts intracellular ROS homeostasis. Notably, high LncFASA expression indicates favorable overall survival in individuals with breast cancer, and LncFASA impairs the growth of breast xenograft tumors by modulating ferroptosis. Together, our findings illustrate the crucial role of this lncRNA in ferroptosis-mediated cancer development and provide new insights into therapeutic strategies for breast cancer. | Xiao Fan Fangzhou Liu Xiang Wang Ying Wang Yu Chen Chengyu Shi Xinwan Su Manman Tan Qingfeng Yan Jinrong Peng Jianzhong Shao Yan Xiong Aifu Lin | 2024 | Science China(Life Sciences)2024，67，3： | 0 |
| 8 | 特异性减少B细胞来源的胞外囊泡提高化疗后的抗肿瘤免疫显示文摘文章简介全身性的免疫抑制极大地影响化疗的抗肿瘤免疫。在这项研究中,研究人员揭示了B细胞通过分泌含有CD39和CD73蛋白的CD19阳性胞外囊泡将化疗后大量凋亡肿瘤细胞释放的ATP水解为腺苷,从而削弱了CD8阳性T细胞的抗肿瘤作用。此外,研究人员发现荷瘤小鼠和患者的血清CD19阳性胞外囊泡升高,而且血清CD19胞外囊泡较少的患者在化疗后预后较好。 | 张方慧 李荣荣 杨云山 Chunhui Shi Yingying Shen Chaojie Lu Yinghu Chen Wu Zhou Aifu Lin 8 Lei Yu Wanjing Zhang Zhenwei Xue 王建莉 蔡志坚 | 2020 | 科学新闻2020，，2： | 0 |
| 9 | Micropeptides translated from putative long non-coding RNAs显示文摘Long non-coding RNAs(lncRNAs)transcribed in mammals and eukaryotes were thought to have no protein coding capability.However,recent studies have suggested that plenty of lncRNAs are mis-annotated and virtually contain coding sequences which are translated into bona fide functional peptides by ribosomal machinery,and these functional peptides are called micropeptides or small peptides.Here we review the rapidly advancing field of micropeptides translated from putative lncRNAs,describe the strategies for their identification,and elucidate their critical roles in many fundamental biological processes.We also discuss the prospects of research in micropeptides and the potential applications of micropeptides. | Junhong Li Lei Qu Lingjie Sang Xinyu Wu Anlan Jiang Jian Liu Aifu Lin | 2022 | Acta Biochimica et Biophysica Sinica2022，54，3： | 0 |
| 10 | AIFM1 variants associated with auditory neuropathy spectrum disorder cause apoptosis due to impaired apoptosis-inducing factor dimerization显示文摘Auditory neuropathy spectrum disorder(ANSD)represents a variety of sensorineural deafness conditions characterized by abnormal inner hair cells and/or auditory nerve function,but with the preservation of outer hair cell function.ANSD represents up to 15%of individuals with hearing impairments.Through mutation screening,bioinformatic analysis and expression studies,we have previously identified several apoptosis-inducing factor(AIF)mitochondria-associated 1(AIFM1)variants in ANSD families and in some other sporadic cases.Here,to elucidate the pathogenic mechanisms underlying each AIFM1 variant,we generated AIF-null cells using the clustered regularly interspersed short palindromic repeats(CRISPR)/CRISPR-associated protein 9(Cas9)system and constructed AIF-wild type(WT)and AIF-mutant(mut)(p.T260A,p.R422W,and p.R451Q)stable transfection cell lines.We then analyzed AIF structure,coenzyme-binding affinity,apoptosis,and other aspects.Results revealed that these variants resulted in impaired dimerization,compromising AIF function.The reduction reaction of AIF variants had proceeded slower than that of AIF-WT.The average levels of AIF dimerization in AIF variant cells were only 34.5%-49.7%of that of AIF-WT cells,resulting in caspase-independent apoptosis.The average percentage of apoptotic cells in the variants was 12.3%-17.9%,which was significantly higher than that(6.9%-7.4%)in controls.However,nicotinamide adenine dinucleotide(NADH)treatment promoted the reduction of apoptosis by rescuing AIF dimerization in AIF variant cells.Our findings show that the impairment of AIF dimerization by AIFM1 variants causes apoptosis contributing to ANSD,and introduce NADH as a potential drug for ANSD treatment.Our results help elucidate the mechanisms of ANSD and may lead to the provision of novel therapies. | YUE QIU HONGYANG WANG HUAYE PAN JING GUAN LEI YAN MINGJIE FAN HUI ZHOU XUANHAO ZHOU KAIWEN WU ZEXIAO JIA QIANQIAN ZHUANG ZHAOYING LEI MENGYAO LI XUE DING AIFU LIN YONG FU DONG ZHANG QIUJU WANG QINGFENG YAN | 2023 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2023，24，2： | 0 |
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