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tumor suppressor p53 cross-talks with TRIM family proteins

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Genes & Diseases 2021年第4期8卷 463-474页

作者： Juan Liu Cen Zhang Xue Wang Wenwei Hu Zhaohui Feng Department of Radiation Oncology Rutgers Cancer Institute of New JerseyRutgers-State University of New Jersey195 Little Albany StreetNew BrunswickNJ 08903USA

p53 is a key tumor *** a transcription factor,p53 accumulates in cells in response to various stress signals and selectively transcribes its target genes to regulate a wide variety of cellular stress responses to exert its function in tumor *** addition to tumor suppression,p53 is also involved in many other physiological and pathological processes,***-infection,immune response,development,reproduction,neurodegeneration and *** maintain its proper function,p53 is under tight and delicate regulation through different mechanisms,particularly the posttranslational *** tripartite motif(TRIM)family proteins are a large group of proteins characterized by the RING,B-Box and coiled-coil(RBCC)domains at the *** proteins play important roles in regulation of many fundamental biological processes,including cell proliferation and death,DNA repair,transcription,and immune *** of TRIM proteins have been linked to many diseases including cancer,infectious diseases,developmental disorders,and ***,recent studies have revealed that many TRIM proteins are involved in the regulation of p53,and at the same time,many TRIM proteins are also regulated by ***,we review the cross-talk between p53 and TRIM proteins,and its impact upon cellular biological processes as well as cancer and other diseases.

关键词： Cancer p53 Posttranslational modification TRIM proteins tumor suppressor Ubiquitination

tumor suppressor p53:new functions of an old protein

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Frontiers in Biology 2011年第1期6卷 58-68页

作者： Zhaohui FENG Rui WU Meihua LIN Wenwei HU Department of Radiation Oncology The Cancer Institute of New JerseyUniversity of Medicine and Dentistry of New JerseyNew BrunswickNJ 08903USA Department of Pediatrics and Department of Obstetrics and Gynecology The Cancer Institute of New JerseyUniversity of Medicine and Dentistry of New JerseyNew BrunswickNJ 08903USA

p53 was discovered 30 years *** studies have been done on p53 since then,which makes p53 one of the most extensively studied genes.p53 has long been recognized as a key tumor *** cycle arrest,apoptosis and senescence have been traditionally recognized as the main functions of p53 in tumor ***,some novel functions of p53 have been identified,including the regulation of energy metabolism,antioxidant defense,and microRNA expression and maturation,which all contribute to the role of p53 in tumor ***,the contribution of p53 to normal biologic processes(*** and aging)and some other aspects of diseases(*** diseases)is only now being *** we will review recent advances in the study of some new functions of p53.

关键词： p53 tumor suppressor energy metabolism oxidative stress microRNAs reproduction

The tumor suppressor kinase LKB1:lessons from mouse models

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分子细胞生物学报:英文版 2011年第6期3卷 330-340页

作者： Saara Ollila Tomi P.Makela Institute of Biotechnology University of HelsinkiViikki BiocenterViikinkaari 9BFIN-00014HelsinkiFinland

Mutations in the tumor suppressor gene LKB1 are important in hereditary Peutz–Jeghers syndrome,as well as in sporadic cancers including lung and cervical ***1 is a kinase-activating kinase,and a number of LKB1-dependent phosphorylation cascades regulate fundamental cellular and organismal processes in at least metabolism,polarity,cytoskeleton organization,and prolifer*** targeting approaches are beginning to demonstrate the relevance and specificity of these signaling pathways in development and homeostasis of multiple *** than one of the pathways also appear to contribute to tumor growth following Lkb1 deficiencies based on a number of mouse tumor ***1-dependent activation of AMPK and subsequent inactivation of mammalian target of rapamycin signaling are implicated in several of the models,and other less well characterized pathways are also *** targeting studies of Lkb1 also point an important role of LKB1 in epithelial–mesenchymal interactions,significantly expanding knowledge on the relevance of LKB1 in human disease.

关键词： LKB1 tumor suppressor mouse model AMPK

KLF4 is a tumor suppressor in anaplastic meningioma stem-like cells and human rneningiomas

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Journal of Molecular Cell Biology 2017年第4期9卷 315-324页

作者： Hailiang Tang Hongda Zhu Xuanchun Wang Lingyang Hua Jingrun Li Qing Xie Xiancheng Chen Tao Zhang Ye Gong Department of Neurosurgery Huashan Hospital Fudan University Shanghai 200040 China Department of Endocrinology Huashan Hospital Fudan University Shanghai 200040 China Department of Laboratory Medicine Huashan Hospital Fudan University Shanghai 200040 China

Meningiomas are the most common primary tumors in central nervous system. While recent studies have revealed genetic clues to lower grade human meningiomas, the molecular determinants driving the progression and recurrence of anaplastic meningi- oma, the most malignant subtype with a low prevalence but high morbidity, are still poorly understood. It has been proposed that high recurrence rates of malignant meningiomas are linked to cancer stem cells. Indeed, tumor stem-Uke cells have been iso- lated from various meningioma subtypes, but never been obtained from anaplastic meningioma, in this study, we successfully isolated stem-Uke cells from human anaplastic meningioma. These cells are capable of forming spheres and initiating xenograft tumors that recapitulate anaplastic meningioma phenotypes, and thus could serve as an in vitro model for malignant meningi- omas. KLF4, a transcription factor known for its role in sternness maintenance, was identified as one of the most frequently mutated genes in the benign secretory meningioma. Interestingly, we found that KLF4 is downregulated in anaplastic meningi- oma compared with low-grade meningioma subtypes. By manipulating KLF4 expression in anaplastic meningioma stem-like cells, we demonstrated that KLF4 acts as a tumor suppressor during malignant progression in meningioma, affecting apoptosis, prolif- eration, invasion, and cell cycle. These results suggest a potential therapeutic value of KLF4 for clinical intervention of anaplastic meningioma.

关键词： anaplastic meningioma KLF4 tumor suppressor cancer stem-like cells stemness maintenance

The functions of tumor suppressor PTEN in innate and adaptive immunity

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Cellular & Molecular Immunology 2017年第7期14卷 581-589页

作者： Lang Chen Deyin Guo Department of Immunology School of Basic Medical SciencesWuhan UniversityWuhan 430071China School of Medicine(Shenzhen) Sun Yat-sen UniversityGuangzhou 510080China

The tumor suppressor phosphatase and tensin homolog(PTEN)is a lipid and protein phosphatase that is able to antagonize the PI3K/AKT pathway and inhibit tumor *** also possesses phosphatase-independent *** alterations of PTEN may lead to the deregulation of cell proliferation,survival,differentiation,energy metabolism and cellular architecture and *** the role of PTEN in tumor suppression is extensively documented and well established,the evidence for its roles in immunity did not start to accumulate until *** this review,we will focus on the newly discovered functions of PTEN in the regulation of innate and adaptive immunity,including antiviral responses.

关键词： adaptive immunity innate immunity PTEN tumor suppressor

SPINOPHILIN: A multiplayer tumor suppressor

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Genes & Diseases 2023年第1期10卷 187-198页

作者： Eva M.Verdugo-Sivianes Amancio Carnero Instituto de Biomedicina de Sevilla IBISHospital Universitario Virgen del RocioConsejo Superior de Investigaciones CientificasUniversidad de SevillaSeville 41013Spain CIBERONC Instituto de Salud Carlos IlMadrid 28029Spain

SPINOPHILIN(SPN,PPP1R9B or NEURABIN-2)is a multifunctional protein that regulates protein-protein interactions in different cell signaling *** is also one of the regulatory subunits of protein phosphatase 1(PP1),implicated in the dephosphorylation of retinoblastoma protein(pRB)during cell *** SPN gene has been described as a tumor suppressor in different human tumor contexts,in which low levels of SPN are correlated with a higher grade and worse *** addition,mutations of the SPN protein have been reported in human ***,an oncogenic mutation of sPN,A566V,was described,which affects both the SPN-PP1 interaction and the phosphatase activity of the holoenzyme,and promotes p53-dependent tumorigenesis by increasing the cancer stem cell(CsC)pool in breast ***,the loss or mutation of SPN could be late events that promotes tumor progression by increasing the CSC pool and,eventually,the malignant behavior of the tumor.

关键词： Cancer therapy Phosphatase PP1 SPINOPHILIN tumor suppressor tumorigenesis

LKB1 in lung cancerigenesis:a serine/threonine kinase as tumor suppressor

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Protein & Cell 2011年第2期2卷 99-107页

作者： Yijun Gao Gaoxiang Ge Hongbin Ji Laboratory of Molecular Cell Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China

Lung cancer is featured with high mortality,with a 15%five-year survival rate *** alterations,such as loss of function of tumor suppressor genes,frequently contribute to lung cancer initiation,progression and *** kinase B1(LKB1),as a serine/threonine kinase and tumor suppressor,is frequently mutated and inactivated in non-small cell lung cancer(NSCLC).Recent studies have provided strong evidences that LKB1 loss promotes lung cancerigenesis process,especially lung cancer progression and *** review will summarize recent progress on how LKB1 modulates the process of lung cancerigenesis,emphasizing on LKB1 downstream signaling pathways and biological *** will further discuss the potential development of prognostic biomarkers or therapeutic targets in lung cancer clinic based on the molecular alteration associated with deregulated LKB1 signaling.

关键词： liver kinase B1 lung cancer tumor suppressor

Identification of a potential tumor suppressor gene, UBL3, in non-small cell lung cancer

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Cancer Biology & Medicine 2020年第1期17卷 76-87页

作者： Xinchun Zhao Yongchun Zhou Qian Hu Sanhui Gao Jie Liu Hong Yu Yanfei Zhang Guizhen Wang Yunchao Huang Guangbiao Zhou School of Life Sciences University of Science and Technology of ChinaHefei 230026China State Key Laboratory of Molecular Oncology National Cancer CenterNational Clinical Research Center for CancerCancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Department of Thoracic Surgery the Third Affiliated Hospital of Kunming Medical UniversityKunming 650106China School of Chinese Materia Medica Beijing University of Chinese MedicineBeijing 100029China

Objective: Oncogenes have been shown to be drivers of non-small cell lung cancer(NSCLC), yet the tumor suppressing genes involved in lung carcinogenesis remain to be systematically investigated. This study aimed to identify tumor suppressing ubiquitin pathway genes(UPGs) that were critical to lung ***: The 696 UPGs were silenced by an siRNA screening in NSCLC cells;the potential tumor suppressing UPGs were analyzed, and their clinical significance was ***: We reported that silencing of 11 UPGs resulted in enhanced proliferation of NSCLC cells, and four UPGs(UBL3, TRIM22, UBE2 G2, and MARCH1) were significantly downregulated in tumor samples compared to that in normal lung tissues and their expression levels were positively associated with overall survival(OS) of NSCLC patients. Among these genes, UBL3 was the most significant one. UBL3 expression was decreased in tumor samples compared to that in paired normal lung tissues in 59/86(68.6%) NSCLCs, was correlated with TNM stage and sex of NSCLC patients, and was significantly higher in non-smoking patients than in smoking patients. Silencing UBL3 accelerated cell proliferation and ectopic expression of UBL3 suppressed NSCLC in vitro and in ***: These results showed that UBL3 represented a tumor suppressor in NSCLC and may have potential for use in therapeutics and for the prediction of clinical outcome of patients.

关键词： Lung cancer ubiquitin pathway genes UBL3 tumor suppressor prognosis

Epithelial protein lost in neoplasm (EPLIN):Beyond a tumor suppressor

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Genes & Diseases 2017年第2期4卷 100-107页

作者： Daqing Wu Georgia Cancer Center and Department of Biochemistry and Molecular Biology Medical College of GeorgiaAugusta UniversityAugustaGAUSA MetCure Therapeutics LLC AtlantaGAUSA

The majority of cancer-related deaths are caused by tumor recurrence,metastasis and therapeutic *** the late stages of tumor progression,multiple factors are involved,including the downregulation and/or loss of function of metastasis *** protein lost in neoplasm(EPLIN),an actin-binding protein,was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial *** evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition(EMT),a crucial process by which cancer cells acquire invasive capabilities and therapeutic ***,downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors,suggesting that EPLIN could be a suppressor of *** this review,I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.

关键词： Actin cytoskeleton Chemoresistance Epithelial-tomesenchymal transition EPLIN Metastasis suppressor tumor suppressor