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Exploring the potential of extrachromosomal DNA as a novel oncogenic driver

Science China Life Sciences 2025年第1期 144-157页

作者： Huanbo Zhu longtao huangfu Junbing Chen Jiafu Ji Xiaofang Xing Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing) Division of Gastrointestinal Cancer Translational Research LaboratoryPeking University Cancer Hospital & Institute Department of Gastrointestinal Cancer Center Peking University Cancer Hospital & Institute Department of Liver Surgery & Transplantation Liver Cancer InstituteZhongshan HospitalFudan University Key Laboratory of Carcinogenesis and Cancer Invasion Ministry of Education State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers Beijing Key Laboratory of Carcinogenesis and Translational ResearchDivision of Gastrointestinal Cancer Translational Research LaboratoryPeking University Cancer Hospital & Institute

Extrachromosomal DNA(ecDNA) is a form of circular DNA mostly found in tumor cells. Unlike the typical chromosomal DNA, ecDNA is circular, self-replicating, and carries complete or partial gene fragments. Although ecDNA occurrence remains a rare event in cancer, recent studies have shown that oncogene amplification on ecDNA is widespread throughout many types of cancer, implying that ecDNA plays a central role in accelerating tumor evolution. ecDNA has also been associated with increased tumor mutation burden, chromosomal instability, and even tumor microenvironment remodeling. ecDNA may be crucial in influencing tumor heterogeneity, drug sensitivity,oncogenic senescence, and tumor immunogenicity, leading to a worsening prognosis for tumor patients. In this way, several clinical trials have been conducted to investigate the importance of ecDNA in clinical treatment. In this review, we summarize the biogenesis, characteristics, and current research methods of ecDNA, discuss the vital role of ecDNA-caused tumor heterogeneity in cancers, and highlight the potential role of ecDNA in cancer therapy.

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SDCBP-AS1 destabilizesβ-catenin by regulating ubiquitination and SUMOylation of hnRNP K to suppress gastric tumorigenicity and metastasis

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Cancer Communications 2022年第11期42卷 1141-1161页

作者： Jing Han Menglin Nie Cong Chen Xiaojing Cheng Ting Guo longtao huangfu Xiaomei Li Hong Du Xiaofang Xing Jiafu Ji Department of Gastrointestinal Cancer Translational Research Laboratory Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer HospitalBeijing Institute for Cancer ResearchBeijing 100142P.R.China Department of Radiation Oncology Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070P.R.China Department of Gastrointestinal Surgery Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer HospitalBeijing Institute for Cancer ResearchBeijing 100142P.R.China

Background:Gastric cancer(GC)is among the most malignant tumors,yet the pathogenesis is not fully understood,especially the lack of detailed information about the mechanisms underlying long non-coding RNA(lncRNA)-mediated post-translational ***,the molecular mechanisms and clinical significance of the novel lncRNA syndecan-binding protein 2-antisense RNA 1(SDCBP2-AS1)in the tumorigenesis and progression of GC were ***:The expression levels of SDCBP2-AS1 in 132 pairs of GC and adjacent normal tissues were compared,and the biological functions were assessed in vitro and in *** pull-down and immunoprecipitation assays were conducted to clarify the interactions of SDCBP2-AS1 and heterogeneous nuclear ribonucleoprotein(hnRNP)***-sequencing,immunoprecipitation,immunofluorescence,and luciferase analyses were performed to investigate the functions of ***:SDCBP2-AS1 was significantly downregulated in GC tissues and pre-dictive of poor patient *** of SDCBP2-AS1 promoted the proliferation and migration of GC cells both in vitro and in ***,SDCBP2-AS1 physically bound to hnRNP K to repress SUMOylation of hnRNP K and facilitated ubiquitination of hnRNP K andβ-catenin,thereby promoting the degradation ofβ-catenin in the *** of SDCBP2-AS1 caused SUMOylation of hnRNP K and stabilizedβ-catenin activity,which altered tran-scription of downstream genes,resulting in tumorigenesis and metastasis of ***,the knockdown of hnRNP K partially abrogated the effects of ***:SDCBP2-AS1 interacts with hnRNP K to suppress tumorigenesis and metastasis of GC and regulates post-transcriptional modifications of hnRNP K to destabilizeβ-*** findings suggest SDCBP2-AS1 as a potential target for the treatment of GC.

关键词： SDCBP2-AS1 gastric cancer hnRNP K β-catenin post-transcriptional modifications tumori-genesis

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TRIM28 promotes the escape of gastric cancer cells from immune surveillance by increasing PD-L1 abundance

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Signal Transduction and Targeted Therapy 2023年第7期8卷 3512-3523页

作者： Xiaoxiao Ma Shuqin Jia Gangjian Wang Min Liang Ting Guo Hong Du Sisi Li Xiaomei Li longtao huangfu Jianping Guo Xiaofang Xing Jiafu Ji Department of Gastrointestinal Cancer Translational Research Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer Hospital&InstituteBeijingChina Department of Molecular Diagnostics Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer Hospital&InstituteBeijingChina Institute of Precision Medicine the First Affiliated HospitalSun Yat-Sen UniversityGuangzhouGuangdong 510275China Department of Gastrointestinal Surgery Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education)Peking University Cancer Hospital&InstituteBeijingChina

Immune checkpoint blockade(ICB)offers a new opportunity for treatment for gastric cancer(G.C.).Understanding the upstream regulation of immune checkpoints is crucial to further improve the efficacy of ICB ***,using the CRISPR-Cas9-based genome-wide screening,we identified TRIM28 as one of the most significant regulators of PD-L1,a checkpoint protein,in ***.

关键词： cancer gastric immune

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Piceatannol enhances Beclin-1 activity to suppress tumor progression and its combination therapy strategy with everolimus in gastric cancer

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Science China(Life Sciences) 2023年第2期66卷 298-312页

作者： longtao huangfu Xiaoyang Wang Shanshan Tian Junbing Chen Xueying Wang Biao Fan Qian Yao Gangjian Wang Cong Chen Jing Han Xiaofang Xing Jiafu Ji Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education) Division of Gastrointestinal Cancer Translational Research LaboratoryPeking University Cancer Hospital&InstituteBeijing 100142China Department of Pharmacy Peking University Cancer Hospital&InstituteBeijing 100142China National Institute on Drug Dependence Peking UniversityBeijing 100191China Gastrointestinal Cancer Center Peking University Cancer Hospital&InstituteBeijing 100142China Department of Pathology Peking University Cancer Hospital&InstituteBeijing 100142China

The effects and regulation of Beclin-1-an autophagy-related protein-have not been fully defined, however, a negative correlation has been reported between Beclin-1 expression and carcinogenesis. Meanwhile, no compound has been shown to directly inhibit its activity. Here, we evaluate piceatannol, a naturally occurring polyphenolic compound, as a potential targeting agonist of Beclin-1, to assess its efficacy as an antitumor agent against gastric cancer. More specifically, we determine the effects of piceatannol treatment on cell viability using a monitoring system and colony forming assay. Piceatannol was found to efficiently inhibit the proliferation of several human gastric cancer cell lines. Autophagic flux is increased by piceatannol treatment, and correlates with inhibition of cell proliferation and colony formation. Additionally, microscale thermophoresis and surface plasmon resonance results show a direct interaction between piceatannol and Beclin-1, which reduces the phosphorylation activity of Beclin-1 at the Ser-295 site. Notably, piceatannol impairs the binding of Beclin-1 to Bcl-2 and enhances the recruitment of binding of UV radiation resistance-associated gene protein, which further triggers Beclin-1-dependent autophagy signaling. An increase in autophagic activity via treatment with the mTOR inhibitor, everolimus, effectively sensitizes piceatannol-induced antitumor effects. Xenograft models confirmed that piceatannol inhibits tumor development and elicits a potent synergistic effect with everolimus in vivo. Taken together, the findings of this study strongly support the application of combinatorial piceatannol and everolimus therapy in future clinical trials for gastric cancer patients.

关键词： piceatannol Beclin-1 autophagy everolimus gastric cancer drug synergy

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Causal relationships between chronotype and risk of multiple cancers by using longitudinal data and Mendelian randomization analysis

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Science China(Life Sciences) 2023年第10期66卷 2433-2436页

作者： Shanshan Tian longtao huangfu Sizhi Ai Junwei Zheng Le Shi Wei Yan Ximei Zhu Qianwen Wang Jiahui Deng Yanping Bao Suhua Chang Lin Lu Peking University Sixth Hospital Peking University Institute of Mental HealthNHC Key Laboratory of Mental Health(Peking University)National Clinical Research Center for Mental Disorders(Peking University Sixth Hospital)Beijing 100191China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education) Division of Gastrointestinal Cancer Translational Research LaboratoryPeking University Cancer Hospital&InstituteBeijing 100142China Department of Cardiology Heart CenterThe First Affiliated Hospital of Xinxiang Medical UniversityXinxiang 453100China National Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Peking UniversityBeijing 100191China Chinese Academy of Medical Sciences Research Unit(No.2018RU006) Peking UniversityBeijing 100191China Peking-Tsinghua Center for Life Sciences PKU-IDG/McGovern Institute for Brain ResearchBeijing 100871China

Dear Editor,Cancer is the second leading cause of death worldwide,and the cancer situation is becoming more complicated(Zhou et al.,2022).The International Agency for Research on Cancer(IARC)Monographs Working Group c... 详细信息

关键词： Cancer death

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小花草玉梅的三萜皂苷成分鉴定及抗肿瘤活性研究

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中国药房 2022年第5期33卷 602-610页

作者：王啸洋吴君皇甫龙韬刘红李雪梅汤海峰张艳华北京大学肿瘤医院暨北京市肿瘤防治研究所药剂科恶性肿瘤发病机制及转化研究教育部重点实验室北京100142 北京大学口腔医院特诊科北京100081 北京大学肿瘤医院暨北京市肿瘤防治研究所胃肠转化研究室恶性肿瘤发病机制及转化研究教育部重点实验室北京100142 空军军医大学药学系/中药与天然药物学教研室西安710032

目的研究银莲花属植物小花草玉梅Anemone rivularis ***-minore的三萜皂苷类化合物及其抗肿瘤活性。方法对该植物根茎的70%乙醇提取物正丁醇萃取部位进行分离,采用正相硅胶柱色谱、反相ODS柱色谱、Sephadex LH-20凝胶柱色谱以及半制备... 详细信息

目的研究银莲花属植物小花草玉梅Anemone rivularis ***-minore的三萜皂苷类化合物及其抗肿瘤活性。方法对该植物根茎的70%乙醇提取物正丁醇萃取部位进行分离,采用正相硅胶柱色谱、反相ODS柱色谱、Sephadex LH-20凝胶柱色谱以及半制备高效液相色谱等手段分离纯化三萜皂苷类化合物;根据波谱(核磁共振谱、质谱)数据及理化性质鉴定化合物结构;采用MTT法检测化合物对5种人源肿瘤细胞(HL-60细胞、A549细胞、HepG2细胞、HeLa细胞和U87MG细胞)的增殖抑制活性;通过流式细胞术Annexin V-FITC/PI双染试验,评估化合物7对U87MG细胞的诱导凋亡作用。结果共分离得到16个三萜皂苷类化合物,分别为3β-O-β-D-吡喃木糖-(1→2)-α-L-吡喃阿拉伯糖-齐墩果酸-28-O-α-L-吡喃鼠李糖-(1→4)-β-D-吡喃葡萄糖-(1→6)-β-D-吡喃葡萄糖酯苷(1)、3β-O-α-L-吡喃阿拉伯糖-齐墩果酸-28-O-β-D-吡喃葡萄糖酯苷(2)、saponin B(3)、齐墩果酸-3β-O-β-D-吡喃葡萄糖-(1→2)-α-L-吡喃阿拉伯糖苷(4)、HN-saponin F(5)、clematoside S(6)、prosapogenin CP4(7)、cussonside B(8)、白头翁皂苷C(9)、clemastanoside D(10)、3β-O-β-D-吡喃葡萄糖-(1→2)-α-L-吡喃阿拉伯糖-常春藤皂苷元-28-O-β-D-吡喃葡萄糖酯苷(11)、刺五加皂苷C3(12)、刺五加皂苷A1(13)、huzhangoside D(14)、刺楸皂苷B(15)和hederacolchisideE(16)。化合物3、4、6~9表现出不同程度的抑制肿瘤细胞增殖活性,并以化合物7的活性最强;化合物7能诱导U87MG细胞凋亡从而抑制肿瘤细胞增殖,并呈一定时间依赖趋势。结论分离所得的16个化合物均为齐墩果烷型三萜皂苷,其中化合物1为新化合物;苷元C-3位连糖基且C-28位为游离羧基的皂苷抗肿瘤活性较强。

关键词：小花草玉梅三萜皂苷鉴定抗肿瘤活性齐墩果烷型三萜皂苷

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