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Snail promotes metastasis of nasopharyngeal carcinoma partly by down-regulating TEL2

Cancer Communications 2018年第1期38卷 622-631页

作者： Yi Sang Chun Cheng Yi-Xin Zeng tiebang kang State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterNo.651 Dongfeng East RoadGuangzhou 510060People’s Republic of China Department of Center Laboratory The Eighth Affiliated Hospital of Sun Yat-Sen UniversityNo.3025 Shennan Middle RoadShenzhen 518033People’s Republic of China Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment The Third Affiliated Hospital of Nanchang UniversityNo.128 Xianshan North RoadNanchang 330008People’s Republic of China

Background:Metastasis is the major cause of treatment failure in patients with nasopharyngeal carcinoma(NPC).We previously reported that TEL2,a negative regulator of SERPINE1,could inhibit NPC metastasis to lymph ***:A series of in vivo and in vitro assays were performed to elucidate the regulation between Snail and ***2 expression was analyzed in three representative NPC cell lines expressing low levels of Snail(S26,6-10B,HK1)and two cell lines expressing high levels of Snail(S18,5-8F).Luciferase and chromatin immunoprecipitation assays were used to analyze the interaction between Snail and *** roles of the Snail/TEL2 pathway in cell migration and invasion of NPC cells were examined using transwell *** to the lungs was examined using nude mouse receiving NPC cells injection through the tail ***:Ectopic Snail expression down-regulated TEL2 at the mRNA and protein levels,whereas knockdown of Snail using short hairpin RNA up-regulated *** and chromatin immunoprecipitation assays indicated that Snail binds directly to the TEL2 *** Snail expression enhanced migration and invasion of NPC cells,and such effects were mitigated by TEL2 ***2 overexpression also attenuated hypoxia-induced cell migration and invasion,and increased the number of metastatic pulmonary *** overexpression reduced the number of metastatic pulmonary ***:TEL2 is a novel target of Snail and suppresses Snail-induced migration,invasion and metastasis in NPC.

关键词： TEL2 Snail Metastasis Nasopharyngeal carcinoma

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Systematic screening for potential therapeutic targets in osteosarcoma through a kinome-wide CRISPR-Cas9 library

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Cancer Biology & Medicine 2020年第3期17卷 782-794页

作者： Yuanzhong Wu Liwen Zhou Zifeng Wang Xin Wang Ruhua Zhang Lisi Zheng tiebang kang Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhou 510060China

Objective:Osteosarcoma is the most common primary malignant bone ***,the survival of patients with osteosarcoma has remained unchanged during the past 30 years,owing to a lack of efficient therapeutic ***:We constructed a kinome-targeting CRISPR-Cas9 library containing 507 kinases and 100 nontargeting controls and screened the potential kinase targets in *** CRISPR screening sequencing data were analyzed with the Model-based Analysis of Genome-wide CRISPR/Cas9 Knockout(MAGeCK)Python *** functional data were applied in the 143B cell line through lenti-CRISPR-mediated gene *** clinical significance of kinases in the survival of patients with osteosarcoma was analyzed in the R2:Genomics Analysis and Visualization ***:We identified 53 potential kinase targets in *** these targets,we analyzed 3 kinases,TRRAP,PKMYT1,and TP53RK,to validate their oncogenic functions in ***1 and TP53RK showed higher expression in osteosarcoma than in normal bone tissue,whereas TRRAP showed no significant *** expression of all 3 kinases was associated with relatively poor prognosis in patients with ***:Our results not only offer potential therapeutic kinase targets in osteosarcoma but also provide a paradigm for functional genetic screening by using a CRISPR-Cas9 library,including target design,library construction,screening workflow,data analysis,and functional *** method may also be useful in potentially accelerating drug discovery for other cancer types.

关键词： Osteosarcoma kinase CRISPR-Cas9 library TRRAP PKMYT1 TP53RK

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Human KIAA1018/FAN1 nuclease is a new mitotic substrate of APC/C^(Cdh1)

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Chinese Journal of Cancer 2012年第9期31卷 440-448页

作者： Fenju Lai Kaishun Hu Yuanzhong Wu Jianjun Tang Yi Sang Jingying Cao tiebang kang State Key Laboratory of Oncology in South China Department of Experimental Research Sun Yat-sen University Cancer CenterGuangzhouGuangdong 510060P.R.China

A recently identified protein, FAN1 (FANCD2-associated nuclease 1, previously known as KIAA1018), is a novel nuclease associated with monoubiquitinated FANCD2 that is required for cellular resistance against DNA interstrand crosslinking (ICL) agents. The mechanisms of FAN1 regulation have not yet been explored. Here, we provide evidence that FAN1 is degraded during mitotic exit, suggesting that FAN1 may be a mitotic substrate of the anaphase-promoting cyclosome complex (APC/C). Indeed, Cdh1, but not Cdc20, was capable of regulating the protein level of FAN1 through the KEN box and the D-box. Moreover, the up-and down-regulation of FAN1 affected the progression to mitotic exit. Collectively, these data suggest that FAN1 may be a new mitotic substrate of APC/C Cdh1 that plays a key role during mitotic exit.

关键词：有丝分裂过程核酸酶基板蛋白质含量人力 DNA链 ICL 泛素化

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Low expression of centrosomal protein 78(CEP78)is associated with poor prognosis of colorectal cancer patients

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Chinese Journal of Cancer 2016年第10期35卷 509-517页

作者： Meifang Zhang Tingmei Duan Li Wang Jianjun Tang Rongzhen Luo Ruhua Zhang tiebang kang State Key Laboratory of Oncology in South China Collaborative Innova-tion Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060GuangdongP.R.China. Department of Pathology Sun Yat-sen University Cancer CenterGuangzhou 510060GuangdongP.R.China. Research Department Sun Yat-sen University Cancer CenterGuang-zhou 510060GuangdongP.R.China.

Background: Centrosomal protein 78(CEP78) has been characterized as a component of the centrosome required for the regulation of centrosome-related events during the cell cycle, but its role in human cancers remains unclear. This study aimed to investigate the role and the clinical value of CEP78 in colorectal cancer(CRC).Methods: Quantitative real-time polymerase chain reaction(q RT-PCR) and immunohistochemistry were performed to examine CEP78 expression in CRC tissues and adjacent noncancerous tissues. The association between CEP78 expression and clinical outcomes of CRC patients was determined. The effect of CEP78 on cell growth was examined in vitro by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT) assay, colony formation, and flow cytometry assays and in vivo using a nude mouse ***: The expression level of CEP78 was significantly lower in tumor tissues than in the adjacent normal tissues(P < 0.01). Low CEP78 expression was significantly associated with poor differentiation(P etastasis(P = 0.003), large tumor size(P = 0.017), lymphatic mtient= 0.034), distant metastasis(P s with low CEP78 expression h= 0.029), and advanced stage(P Meier analysis indicated that paad shorter survival than those wit= 0.011). Kaplan–h high CEP78 expression(P < 0.01). Overexpression of CEP78 in CRC cells significantly reduced cell viability and colony formation in vitro and halted tumor growth in vivo. Further study showed that CEP78 reintroduction in CRC cells resulted in G2/M phase arrest rather than cell ***: CEP78 might function as a tumor suppressor and serve as a novel prognostic marker in CRC.

关键词：中心体蛋白结直肠癌预后患者细胞周期聚合酶链反应 RT-PCR 实验检测

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Protein stability regulators screeningassay (Pro-SRSA)： protein degradation meets theCRISPR-Cas9 library

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Chinese Journal of Cancer 2016年第8期35卷 385-387页

作者： Yuanzhong Wu tiebang kang Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer Medicine651 Dongfeng Road EastGuangzhou 510060GuangdongPR.China

The regulation of protein stability is a fundamental issue for biophysical processes,but there has not previously been a convenient and unbiased method of identifying regulators of protein ***,as reported in the article entitled "A genome-scale CRISPR-Cas9 screening method for protein stability reveals novel regulators of Cdc25 A," recently published in Cell Discovery,our team developed a protein stability regulators screening assay(Pro-SRSA) by combining the whole-genome clustered regularly interspaced short palindromic repeats Cas9(CRISPR-Cas9) library with a dual-fluorescence-based protein stability reporter and high-throughput sequencing to screen for regulators of protein *** on our findings,we are confident that this efficient and unbiased screening method at the genome scale will be used by researchers worldwide to identify regulators of protein stability.

关键词： CRISPR-Cas9 screening, Protein stability, Cdc25A, Ubiquitination, Acetylation

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SUMOylation stabilizes hSSB1 and enhances the recruitment of NBS1 to DNA damage sites

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1516-1527页

作者： Liwen Zhou Lisi Zheng Kaishun Hu Xin Wang Ruhua Zhang Yezi Zou Li Zhong Shang Wang Yuanzhong Wu tiebang kang Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhou 510060China Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research CenterSun Yat-sen Memorial HospitalSun Yat‐sen UniversityGuangzhouChina

Human single-stranded DNA-binding protein 1(hSSB1)is required for the efficient recruitment of the MRN complex to DNA doublestrand breaks and is essential for the maintenance of genome ***,the mechanism by which hSSB1 recruits NBS1 remains ***,we determined that hSSB1 undergoes SUMOylation at both K79 and K94 under normal conditions and that this modification is dramatically enhanced in response to DNA *** of hSSB1,which is specifically fine-tuned by PIAS2α,and SENP2,not only stabilizes the protein but also enhances the recruitment of NBS1 to DNA damage *** with defective hSSB1 SUMOylation are sensitive to ionizing radiation,and global inhibition of SUMOylation by either knocking out UBC9 or adding SUMOylation inhibitors significantly enhances the sensitivity of cancer cells to *** findings reveal that SUMOylation,as a novel posttranslational modification of hSSB1,is critical for the functions of this protein,indicating that the use of SUMOylation inhibitors(e.g.,2-D08 and ML-792)may be a new strategy that would benefit cancer patients being treated with chemo-or radiotherapy.

关键词： SSB1 damage NBS1

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RMI2 plays crucial roles in growth and metastasis of lung cancer

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Signal Transduction and Targeted Therapy 2020年第1期5卷 907-909页

作者： Weixiang Zhan Yina Liu Ying Gao Run Gong Wen Wang Ruhua Zhang Yuanzhong Wu tiebang kang Denghui Wei State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer Center510060 GuangzhouChina The Sixth Affiliated Hospital Sun Yat-sen University510000 GuangzhouChina Department of Abdominal Oncology The Cancer Center of the Fifth Affiliated Hospital of Sun Yat-sen University519000 ZhuhaiGuangdongChina

Dear Editor,Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer death in the world,but its therapeutic targets are still being *** instability as a key hallmark of cancer not only contributes to cancer initiation and progression,1 but also creates vulnerabilities that are relatively specific to cancer cells,which may be potential therapeutic targets for cancer *** DNA Double-Strand Breaks(DSBs)repair,BTR(BLM-Topo IIIα-RMI1/RMI2)complex promotes the dissolution of double Holliday junctions to form non-crossover products and is often considered as a tumor suppressor.2 However,the function of each individual component of this BTR complex in cancer remains largely unknown.

关键词： cancer metastasis Lung

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KIF2C:a novel link between Wnt/β-catenin and mTORCI signaling in the pathogenesis of hepatocellular carcinoma

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Protein & Cell 2021年第10期12卷 788-809页

作者： Shi Wei Miaomiao Dai Chi Zhang Kai Teng Fengwei Wang Hongbo Li Weipeng Sun Zihao Feng tiebang kang Xinyuan Guan Ruihua Xu Muyan Cai Dan Xie State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China Department of Radiation Oncology Shandong Cancer Hospital and InstituteShandong First Medical University and Shandong Academy of Medical SciencesJinan 250200China Department of Musculoskeletal Oncology the First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Anorectal Surgery the First Affiliated Hospital of Zhengzhou UniversityZhengzhou 510370China Department of Urology the First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Clinical Oncology Li Ka Shing Faculty of MedicineThe University of Hong KongPokfulamHong Kong SARChina Department of Pathology Sun Yat-sen University Cancer CenterGuangzhou 510060China

Hepatocellular carcinoma(HCC)is the most common primary liver malignancy and is the fourth-leading cause of cancer-related deaths *** is refractory to many standard cancer treatments and the prognosis is often poor,highlighting a pressing need to identify biomarkers of aggressiveness and potential targets for future *** family member 2C(KIF2C)is reported to be highly expressed in several human ***,the molecular mechanisms underlying the role of KIF2C in tumor development and progression have not been *** this study,we found that KIF2C expression was significantly upregulated in HCC,and that KIF2C up-regulation was associated with a poor *** both gain and loss of function assays,we showed that KIF2C promoted HCC cell proliferation,migration,invasion,and metastasis both in vitro and in ***,we identified TBC1D7 as a binding partner of KIF2C,and this interaction disrupts the formation of the TSC complex,resulting in the enhancement of mammalian target of rapamycin complexl(mTORCI)signal ***,we found that KIF2C is a direct target of the Wnt/β-catenin pathway,and acts as a key factor in mediating the crosstalk between Wnt/β-catenin and mTORCI ***,the results of our study establish a link between Wnt/β-catenin and mTORCI signaling,which highlights the potential of KIF2C as a therapeutic target for the treatment of HCC.

关键词： KIF2C HCC TBC1D7 mTORCI signaling Wnt/β-catenin signaling

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Cannabis suppresses antitumor immunity by inhibiting JAK/STAT signaling in T cells through CNR2

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Signal Transduction and Targeted Therapy 2022年第5期7卷 1657-1669页

作者： Xinxin Xiong Siyu Chen Jianfei Shen Hua You Han Yang Chao Yan Ziqian Fang Jianeng Zhang Xiuyu Cai Xingjun Dong tiebang kang Wende Li Penghui Zhou State Key Laboratory of Oncology in Southern China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China Guangdong Provincial People’s Hospital Guangdong Academy of Medical SciencesGuangzhou 510515China Guangdong Laboratory Animals Monitoring Institute Guangdong Key Laboratory of Laboratory AnimalsGuangzhou 510663China Department of Thoracic Surgery Taizhou Hospital of Zhejiang ProvinceWenzhou Medical UniversityLinhai 317000China Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou 510095China Department of Thoracic Surgery Sun Yat-sen University Cancer CenterGuangzhou 510060China State Key Laboratory of Pharmaceutical Biotechnology Nanjing UniversityNanjing 210023China

The combination of immune checkpoint blockade(ICB)with chemotherapy significantly improves clinical benefit of cancer *** chemotherapy is often associated with adverse events,concomitant treatment with drugs managing side effects of chemotherapy is frequently used in the combination ***,whether these ancillary drugs could impede immunotherapy remains ***,we showed that∆9-tetrahydrocannabinol(THC),the key ingredient of drugs approved for the treatment of chemotherapy-caused nausea,reduced the therapeutic effect of PD-1 *** endogenous cannabinoid anandamide(AEA)also impeded antitumor immunity,indicating an immunosuppressive role of the endogenous cannabinoid system(ECS).

关键词： JAK/STAT drugs chemotherapy treatment

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MFN2 suppresses clear cell renal cell carcinoma progression by modulating mitochondria-dependent dephosphorylation of EGFR

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Cancer Communications 2023年第7期43卷 808-833页

作者： Li Luo Denghui Wei Yihui Pan Qiu-Xia Wang Jian-Xiong Feng Bing Yu tiebang kang Junhang Luo Jiefeng Yang Song Gao State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhouGuangdongP.R.China Department of Urology The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongP.R.China Department of Urology The Third Affiliated Hospital of Soochow UniversityChangzhouJiangsuP.R.China

Background:Clear cell renal cell carcinoma(ccRCC)is the most lethal renal *** overwhelming increase of patients experience tumor progression and unfavorable ***,the molecular events underlying ccRCC tumorigenesis and metastasis remain ***,uncovering the underlying mechanisms will pave the way for developing novel therapeutic targets for *** this study,we sought to investigate the role of mitofusin-2(MFN2)in supressing ccRCC tumorigenesis and ***:The expression pattern and clinical significance of MFN2 in ccRCC were analyzed by using the Cancer Genome Atlas datasets and samples from our independent ccRCC *** in vitro and in vivo experiments,including cell proliferation,xenograft mouse models and transgenic mouse model,were used to determine the role of MFN2 in regulating the malignant behaviors of ***-sequencing,mass spectrum analysis,co-immunoprecipitation,bio-layer interferometry and immunofluorescence were employed to elucidate the molecular mechanisms for the tumor-supressing role of ***:we reported a tumor-suppressing pathway in ccRCC,characterized by mitochondria-dependent inactivation of epidermal growth factor receptor(EGFR)*** process was mediated by the outer mitochondrial membrane(OMM)protein ***2 was down-regulated in ccRCC and associated with favorable prognosis of ccRCC *** vivo and in vitro assays demonstrated thatMFN2 inhibited ccRCC tumor growth and metastasis by suppressing the EGFR signaling *** a kidney-specific knockout mouse model,loss of MFN2 led to EGFR pathway activation and malignant lesions in ***,MFN2 preferably binded small GTPaseRab21 in its GTPloading form,which was colocalized with endocytosed EGFR in ccRCC *** this EGFR-Rab21-MFN2 interaction,endocytosed EGFR was docked to mitochondria and subsequently dephosphorylated by the OMM-residing tyrosine-protein phosphatase receptor type J(PTPRJ).Conclusion

关键词： ccRCC EGFR signaling pathway MFN2 PTPRJ Rab21

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