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Major roles of the circadian clock in cancer

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Cancer Biology & Medicine 2023年第1期20卷 1-24页

作者： Chen Huang Chenliang Zhang Yubin Cao Jian Li Feng Bi Department of Abdominal oncology Cancer Center and Laboratory of Molecular Targeted Therapy in OncologyWest China HospitalSichuan UniversityChengdu 610000China laboratory of molecular Targeted Therapy in oncology West China HospitalSichuan UniversityChengdu 610000China Department of Gastroenterology West China HospitalSichuan UniversityChengdu 610000China West China School of Medicine Sichuan UniversityChengdu 610000China

Circadian rhythms are natural rhythms that widely exist in all creatures,and regulate the processes and physiological functions of various biochemical reactions.The circadian clock is critical for cancer occurrence and progression.Its function is regulated by metabolic activities,and the expression and transcription of various genes.This review summarizes the composition of the circadian clock;the biological basis for its function;its relationship with,and mechanisms in,cancer;its various functions in different cancers;the effects of anti-tumor treatment;and potential therapeutic targets.Research in this area is expected to advance understanding of circadian locomotor output cycles kaput(CLOCK)and brain and muscle ARNT-like protein 1(BMAL1)in tumor diseases,and contribute to the development of new anti-tumor treatment strategies.

关键词： Circadian clock BMAL1 cancer tumor therapy oncology

Epstein-Barr virus is associated with gastric carcinoma: The question is what is the significance?

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World Journal of Gastroenterology 2008年第27期14卷 4347-4351页

作者： Hugo Sousa Ana L Pinto-Correia Rui Medeiros Mario Dinis-Ribeiro molecular oncology Group and molecular Virology laboratory Portuguese Institute of Oncology of Porto Gastroenterology Department Portuguese Institute of Oncology of Porto

AIM: To examine the possible role of the Epstein- Barr Virus (EBV) in the development of gastric adenocarcinoma (GC). It is unclear whether EBV is involved in GC development or is a consequence of gastric inflammation secondary to immunosuppressive treatments. METHODS: A systematic review was carried out of all published observational studies on the temporal association between EBV and GC, with a view to determine a causal relationship. RESULTS: The present study showed that the worldwide crude prevalence of EBV in gastric adenocarcinoma was 8.29%. The prevalence varied from 7.08% for intestinal type and 9.82% for diffuse type of GC. It was observed that Western and Central Asian countries had a significantly higher frequency of EBV positive cases compared to South-Eastern countries. America had the highest EBV-GC prevalence whereas Europe had the lowest. CONCLUSION: The present review has demonstrated a high prevalence of EBV in gastric adenocarcinoma. However, studies designed to assess a temporal relationship and histological association using sensitive techniques should be carried out to establish the role of EBV in GC carcinogenesis.

关键词：胃癌 Epstein-Barr病毒系统观查胃炎

Deregulated expression and subcellular localization of CPSF6,a circRNA-binding protein,promote malignant development of esophageal squamous cell carcinoma

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Chinese Journal of Cancer Research 2022年第1期34卷 11-27页

作者： Shichao Guo Guangchao Wang Zitong Zhao Dan Li Yongmei Song Qimin Zhan State Key Laboratory of Molecular Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Key laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142China

Objective:Cleavage and polyadenylation specific factor 6(CPSF6)has been documented as an oncoprotein in different types of cancer.However,functions of CPSF6 have not been investigated yet in esophageal squamous cell carcinoma(ESCC).Here,we aimed to investigate the potential clinical values and biological functions of CPSF6 in ESCC.Methods:For determining the expression level of CPSF6 in ESCC patients,we analyzed published data,performed quantitative real-time polymerase chain reaction(RT-qPCR)and immunohistochemistry assays.Kaplan-Meier curves and log-rank tests were used for survival analyses.GO and KEGG analyses were done for CPSF6-related genes.Cell proliferation,colony formation and xenograft assays were conducted to verify the effects of CPSF6 on ESCC.In addition,cell cycle and apoptosis assays were also performed to manifest the functions of CPSF6 and circCPSF6.RNA pulldown and radioimmunoprecipitation(RIP)assays were used for confirming the interaction between circCPSF6(hsa_circ_0000417)and CPSF6 protein.The regulatory relationship between CPSF6 protein and circCPSF6 was determined by RT-qPCR.Results:We found that CPSF6 was upregulated in ESCC tissues and overexpression of cytoplasmic CPSF6 was associated with poor prognosis.GO and KEGG analyses suggested that CPSF6 could mainly affect cell division in ESCC.Further experiments manifested that CPSF6 promoted cell proliferation and colony formation in vitro.Xenograft assay showed that knockdown of CPSF6 significantly decreased tumor growth rate in vivo.Subsequently,we verified that depletion of CPSF6 led to cell cycle arrest and apoptosis.Finally,we validated that CPSF6,as a circRNA-binding protein,interacted with and regulated its circular isoform circCPSF6(hsa_circ_0000417),of which depletion also resulted in cell cycle arrest and cell apoptosis in ESCC.Conclusions:These findings gave us insight that overexpression of cytoplasmic CPSF6 protein is associated with poor prognosis in ESCC and CPSF6 may function as an oncoprotein,at least in part,through regula

关键词： CPSF6 esophageal squamous cell carcinoma prognosis cell proliferation circRNA-binding protein circCPSF6

Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma(ESCC)

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Acta Pharmaceutica Sinica B 2021年第1期11卷 143-155页

作者： Jie Cheny Yan Wangy Di Zhao Lingyuan Zhang Weimin Zhang Jiawen Fan Jinting Li Qimin Zhan Key laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&InstituteBeijing 100142China

Among current novel druggable targets,proteineprotein interactions(PPIs)are of considerable and growing interest.Diacylglycerol kinase a(DGKα)interacts with focal adhesion kinase(FAK)band 4.1-ezrin-radixin-moesin(FERM)domain to induce the phosphorylation of FAK Tyr397 site and promotes the malignant progression of esophageal squamous cell carcinoma(ESCC)cells.Chrysin is a multi-functional bioactive flavonoid,and possesses potential anticancer activity,whereas little is known about the anticancer activity and exact molecular mechanisms of chrysin in ESCC treatment.In this study,we found that chrysin significantly disrupted the DGKα/FAK signalosome to inhibit FAKcontrolled signaling pathways and the malignant progression of ESCC cells both in vitro and in vivo,whereas produced no toxicity to the normal cells.molecular validation specifically demonstrated that Asp435 site in the catalytic domain of DGKαcontributed to chrysin-mediated inhibition of the assembly of DGKα/FAK complex.This study has illustrated DGKα/FAK complex as a target of chrysin for the first time,and provided a direction for the development of natural products-derived PPIs inhibitors in tumor treatment.

关键词： Chrysin Esophageal squamous cell carcinoma DGKα FAK Proteineprotein interactions

Improved method increases sensitivity for circulating hepatocellular carcinoma cells

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World Journal of Gastroenterology 2015年第10期21卷 2918-2925页

作者： Hui-Ying Liu Hai-Hua Qian Xiao-Feng Zhang Jun Li Xia Yang Bin Sun Jun-Yong Ma Lei Chen Zheng-Feng Yin molecular oncology laboratory Eastern Hepatobiliary Surgery HospitalSecond Military Medical University

AIM:To improve an asialoglycoprotein receptor(ASGPR)-based enrichment method for detection of circulating tumor cells(CTCs)of hepatocellular carcinoma(HCC).METHODS:Peripheral blood samples were collected from healthy subjects,patients with HCC or various other cancers,and patients with hepatic lesions or hepatitis.CTCs were enriched from whole blood by extracting CD45-expressing leukocytes with monoclonal antibody coated-beads following density gradient centrifugation.The remaining cells were cytocentrifuged on polylysine-coated slides.Isolated cells were treated by triple immunofluorescence staining with CD45antibody and a combination of antibodies against ASGPR and carbamoyl phosphate synthetase 1(CPS1),used as liver-specific markers,and costained with DAPI.The cell slide was imaged and stained tumor cells that met preset criteria were counted.Recovery,sensitivity and specificity of the detection methods were determined and compared by spiking experiments with various types of cultured human tumor cell lines.Expression of ASGPR and CPS1 in cultured tumor cells and tumor tissue specimens was analyzed by flow cytometry and triple immunofluorescence staining,respectively.RESULTS:CD45 depletion of leukocytes resulted in a significantly greater recovery of multiple amounts of spiked HCC cells than the ASGPR+selection(P s<0.05).The expression rates of either ASGPR or CPS1were different in various liver cancer cell lines,ranging between 18%and 99%for ASGPR and between 9%and 98%for CPS1.In both human HCC tissues and liver cancer cell lines,there were a few HCC cells that did not stain positive for ASGPR or CPS1.The mixture of monoclonal antibodies against ASGPR and CPS1identified more HCC cells than either antibody alone.However,these antibodies did not detect any tumor cells in blood samples spiked with the human breastcancer cell line MCF-7 and the human renal cancer cell line A498.ASGPR+or/and CPS1+CTCs were detected in 29/32(91%)patients with HCC,but not in patients with any other kind of cancer or any of the other

关键词： Asialoglycoprotein receptor Carbamoyl phosphate sy

Treatment of advanced non-small cell lung cancer with driver mutations: current applications and future directions

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Frontiers of Medicine 2023年第1期17卷 18-42页

作者： Jia Zhong Hua Bai Zhijie Wang Jianchun Duan Wei Zhuang Di Wang Rui Wan Jiachen Xu Kailun Fei Zixiao Ma Xue Zhang Jie Wang State Key Laboratory of Molecular Oncology Department of Medical OncologyNational Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China

With the improved understanding of driver mutations in non-small cell lung cancer (NSCLC), expanding the targeted therapeutic options improved the survival and safety. However, responses to these agents are commonly temporary and incomplete. Moreover, even patients with the same oncogenic driver gene can respond diversely to the same agent. Furthermore, the therapeutic role of immune-checkpoint inhibitors (ICIs) in oncogene-driven NSCLC remains unclear. Therefore, this review aimed to classify the management of NSCLC with driver mutations based on the gene subtype, concomitant mutation, and dynamic alternation. Then, we provide an overview of the resistant mechanism of target therapy occurring in targeted alternations (“target-dependent resistance”) and in the parallel and downstream pathways (“target-independent resistance”). Thirdly, we discuss the effectiveness of ICIs for NSCLC with driver mutations and the combined therapeutic approaches that might reverse the immunosuppressive tumor immune microenvironment. Finally, we listed the emerging treatment strategies for the new oncogenic alternations, and proposed the perspective of NSCLC with driver mutations. This review will guide clinicians to design tailored treatments for NSCLC with driver mutations.

关键词： non-small cell lung cancer driver mutations treatment strategy resistant mechanism immune-checkpoint inhibitors

Exosomes rewire the cartilage microenvironment in osteoarthritis:from intercellular communication to therapeutic strategies

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International Journal of Oral Science 2022年第3期14卷 259-274页

作者： Yuangang Wu Jiao Li Yi Zeng Wenchen Pu Xiaoyu Mu Kaibo Sun Yong Peng Bin Shen Orthopedic Research Institute Department of OrthopedicsWest China HospitalSichuan UniversityChengduChina Laboratory of Molecular Oncology Frontiers Science Center for Disease-related Molecular NetworkState Key Laboratory of Biotherapy and Cancer CenterWest China HospitalSichuan UniversityChengduChina

Osteoarthritis(OA)is a prevalent degenerative joint disease characterized by cartilage loss and accounts for a major source of pain and disability worldwide.However,effective strategies for cartilage repair are lacking,and patients with advanced OA usually need joint replacement.Better comprehending OA pathogenesis may lead to transformative therapeutics.Recently studies have reported that exosomes act as a new means of cell-to-cell communication by delivering multiple bioactive molecules to create a particular microenvironment that tunes cartilage behavior.Specifically,exosome cargos,such as noncoding RNAs(ncRNAs)and proteins,play a crucial role in OA progression by regulating the proliferation,apoptosis,autophagy,and inflammatory response of joint cells,rendering them promising candidates for OA monitoring and treatment.This review systematically summarizes the current insight regarding the biogenesis and function of exosomes and their potential as therapeutic tools targeting cell-to-cell communication in OA,suggesting new realms to improve OA management.

关键词： Exosomes rewire the cartilage microenvironment in osteoarthritis from intercellular communication to therapeutic strategies

Cysteine-113 covalency inspires the development of Pin1 inhibitor

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Signal Transduction and Targeted Therapy 2020年第1期5卷 643-645页

作者： Wenchen Pu Jiao Li Yong Peng Laboratory of Molecular Oncology Frontiers Science Center for Disease-related Molecular NetworkState Key Laboratory of Biotherapy and Cancer CenterWest China HospitalSichuan UniversityChengdu 610064China

Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1(Pin1)controls the functional switch of phosphoproteins and plays an oncogenic role in human cancer,but the discovery of effective Pin1 inhibitors remains challenging.A recent study by Pinch et al.developed a novel Pin1 inhibitor by endowing molecule with covalent reactivity toward Pin1 cysteine-113,1 providing new insights into the design of anticancer Pin1 inhibitors.

关键词： Pin1 al insight

Membranous NOX5-derived ROS oxidizes and activates local Src to promote malignancy of tumor cells

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1111-1122页

作者： Jie Chen Yan Wang Weimin Zhang Di Zhao Lingyuan Zhang Jiawen Fan Jinting Li Qimin Zhan Key laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Laboratory of Molecular OncologyPeking University Cancer Hospital&Institute100142 BeijingChina

Reactive oxygen species(ROS)localized at the precise subcellular compartments are essential for regulating the activity of signaling proteins.Furthermore,ROS are master regulators of tumor malignant progression that respond to a diverse set of environmental stress,especially hypoxia.NADPH oxidases(NOXs)appear to be activated within discrete subcellular compartments to facilitate local ROS production.However,the subcellular function of NOXs in hypoxic tumor is still unclear.In this study,we demonstrated that NOX5 was greatly upregulated in clinical esophageal squamous cell carcinoma(ESCC)tumors,ESCC cell lines or primary ESCC cells,and elevated NOX5 was correlated to malignancy of ESCC tumors and poor prognosis.NOX5 induced the malignant progression of ESCC by activating Src,especially under hypoxic condition.Mechanistically,we showed that hypoxia promoted the interaction between NOX5 and Pyk2 on cell membrane via facilitating Ca^(2+)-mediated Pyk2 Tyr^(402)site phosphorylation.Subsequently,Pyk2 acted as a scaffold for c-Abl phosphorylating the catalytic domain of NOX5 Tyr^(476/478)sites,which in turn upregulated hydrogen peroxide(H_(2)O_(2))inside the Pyk2/NOX5 complex to oxidize and activate local Src.These findings provide insights into the biological significance of NOX5 in the development of ESCC.

关键词： malignancy elevated esophageal