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Proteomics of adjacent-to-tumor samples uncovers clinically relevant biological events in hepatocellular carcinoma

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National Science Review 2023年第8期10卷 88-104页

作者： Hongwen Zhu Youpei Lin Dayun Lu Shisheng Wang Yuejia Liu Liangqing Dong Qian Meng Jing Gao Yuqiu Wang Nixue Song Yuying Suo Li Ding Pei Wang Bing Zhang Daming Gao Jia Fan Qiang Gao Hu Zhou Department of Analytical Chemistry State Key Laboratory of Drug Research and CAS Key Laboratory of Receptor ResearchShanghai Institute of Materia Medica Chinese Academy of Sciences 2. Department of Liver Surgery and TransplantationLiver Cancer InstituteZhongshan Hospital and Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education Fudan University School of Chinese Materia Medica Nanjing University of Chinese Medicine Institutes for Systems Genetics and NHC Key Lab of Transplant Engineering and Immunology Sichuan Provincial Engineering Laboratory of Pathology in Clinical Application West China Hospital Sichuan University University of Chinese Academy of Sciences Department of Medicine McDonnell Genome Institute Siteman Cancer Center Washington University Department of Genetics and Genomic Sciences Icahn School of Medicine at Mount Sinai lester and sue smith breast center Department of Molecular and Human Genetics Baylor College of Medicine State Key Laboratory of Cell Biology CAS Center for Excellence in Molecular Cell Science Shanghai Institute of Biochemistry and Cell Biology Chinese Academy of Sciences

Normal adjacent tissues(NATs) of hepatocellular carcinoma(HCC) differ from healthy liver tissues and their heterogeneity may contain biological information associated with disease occurrence and clinical outcome that has yet to be fully evaluated at the proteomic level. This study provides a detailed description of the heterogeneity of NATs and the differences between NATs and healthy livers and revealed that molecular features of tumor subgroups in HCC were partially reflected in their respective NATs. Proteomic data classified HCC NATs into two subtypes(Subtypes 1 and 2), and Subtype 2 was associated with poor prognosis and high-risk recurrence. The pathway and immune features of these two subtypes were characterized. Proteomic differences between the two NAT subtypes and healthy liver tissues were further investigated using data-independent acquisition mass spectrometry, revealing the early molecular alterations associated with the progression from healthy livers to NATs. This study provides a high-quality resource for HCC researchers and clinicians and may significantly expand the knowledge of tumor NATs to eventually benefit clinical practice.

关键词： proteomics hepatocellular carcinoma normal tissue adjacent to tumor heterogeneity

Generation of a tree shrew breast cancer model using lentivirus expressing PIK3CA-H1047R

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Zoological Research 2023年第1期44卷 94-97页

作者： Li Zeng Hong-Yan Zhang Chuan-Yu Yang Zhuo Cheng Qiu-Yun Jiang Yao Luo Yi Li Fu-Bing Li Ce-Shi Chen Key Laboratory of Animal Models and Human Disease Mechanisms Kunming Institute of ZoologyChinese Academy of SciencesKunmingYunnan 650223China Faculty of Life Science and Technology Kunming University of Science and TechnologyKunmingYunnan 650500China lester and sue smith breast center Baylor College of MedicineHouston TX 77030USA Academy of Biomedical Engineering Kunming Medical UniversityKunmingYunnan 650500China Third Affiliated Hospital Kunming Medical UniversityKunmingYunnan 650118China Kunming College of Life Science University of Chinese Academy of SciencesKunmingYunnan 650204China

DEAR EDITOR,breast cancer is the most common malignant tumor in women,posing a serious threat to health. Tree shrews(Tupaia belangeri chinensis) are evolutionarily closer to humans than rodents and are emerging as an attractive experimental animal model for breast cancer. The PIK3CA gene is frequently mutated in both human and tree shrew breast tumors. Herein, we effectively overexpressed PIK3CA-H1047R in the mammary epithelial cells of tree shrews using a lentivirus to induce breast tumors.

关键词： PIK3CA breast cancer

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Mapping bone marrow niches of disseminated tumor cells

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Science China(Life Sciences) 2017年第10期60卷 1125-1132页

作者： Weijie Zhang Hin Ching Lo Xiang H.-F.Zhang lester and sue smith breast center Baylor College of Medicine Houston TX 77030 USA Dan L. Duncan Cancer center Baylor College of Medicine Houston TX 77030 USA Department of Molecular and Cellular Biology Baylor College of Medicine Houston TX 77030 USA Graduate Program in Integrative Molecular and Biomedical Sciences Baylor College of Medicine Houston TX 77030 USA McNair Medical Institute Baylor College of Medicine Houston TX 77030 USA

breast cancer cells may disseminate early, before tumor diagnosis. Disseminated tumor cells, or DTCs, reside in the bone marrow, and may persist for years or even decades. Some of these cells may be re-activated to resume aggressive growth, and eventually become overt bone metastases. Recent studies have begun to shed light on this complicated process and revealed multiple steps and intermediate states of colonizing DTCs. However, how cancer-host interactions evolve during this process needs to be further understood. Most of our current knowledge of the bone microenvironment is obtained through studies looking for the hematopoietic stem cell(HSC) niche. Although this long-standing question has not yet been resolved, our search for the HSC niche has resulted in a detailed map of various cell types in the bone marrow. Furthermore, various techniques used to find the HSC niche may also be adapted for finding the cancer cell niche. In this article, we will review the recent progress in both the DTC and HSC areas with a focus on their potential microenvironment niches. We will also discuss how to apply what we have learned from HSC studies to map DTCs in the bone context. We hope to stimulate thoughts and ideas to further elucidate the bone colonization process, and develop potential therapeutic interventions.

关键词： disseminated tumor cells bone marrow niches hematopoietic stem cell niches 3D imaging

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H3K36 methyltransferase NSD1 regulates chondrocyte differentiation for skeletal development and fracture repair

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Bone Research 2021年第3期9卷 349-359页

作者： Rui Shao Zhong Zhang Zhan Xu Huiling Ouyang Lijun Wang Hongwei Ouyang Matthew Greenblatt Xi Chen Weiguo Zou Shanghai Institute of Microsurgery on Extremities and Department of Orthopedic SurgeryShanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell SciencesChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghaiChina Dr.Li Dak Sum&Yip Yio Chin center for Stem Cell and Regenerative Medicine Zhejiang University-University of Edinburgh InstituteZhejiang UniversityHangzhouZhejiangChina China Orthopedic Regenerative Medicine Group HangzhouZhejiangChina Department of Pathology and Laboratory Medicine Weill Cornell MedicineNew YorkNYUSA Department of Molecular and Cellular Biology Lester and Sue Smith Breast CenterDan L.Duncan Cancer CenterBaylor College of MedicineHoustonTXUSA

Chondrocyte differentiation is a critical process for endochondral ossification,which is responsible for long bone development and fracture repair.Considerable progress has been made in understanding the transcriptional control of chondrocyte differentiation;however,epigenetic regulation of chondrocyte differentiation remains to be further studied.NSD1 is a H3K36(histone H3 at lysine 36)methyltransferase.Here,we showed that mice with Nsd1 deficiency in Prx1+mesenchymal progenitors but not in Col2+chondrocytes showed impaired skeletal growth and fracture healing accompanied by decreased chondrogenic differentiation.Via combined RNA sequencing(RNA-seq)and chromatin immunoprecipitation sequencing(ChIP-seq)analysis,we identified sex determining region Y box 9(Sox9),the key transcription factor of chondrogenic differentiation,as a functional target gene of NSD1.Mechanistically,NSD1 regulates Sox9 expression by modulating H3K36me1 and H3K36me2 levels in the Sox9 promoter region,constituting a novel epigenetic regulatory mechanism of chondrogenesis.Moreover,we found that NSD1 can directly activate the expression of hypoxia-inducible factor 1α(HIF1α),which plays a vital role in chondrogenic differentiation through its regulation of Sox9 expression.Collectively,the results of our study reveal crucial roles of NSD1 in regulating chondrogenic differentiation,skeletal growth,and fracture repair and expand our understanding of the function of epigenetic regulation in chondrogenesis and skeletal biology.

关键词： skeletal impaired healing

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ESR1 alterations and metastasis in estrogen receptor positive breast cancer

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Journal of Cancer Metastasis and Treatment 2019年第5期4卷 16-31页

作者： Jonathan T.Lei Xuxu Gou Sinem Seker Matthew J.Ellis Interdepartmental Graduate Program in Translational Biology&Molecular Medicine Baylor College of MedicineHoustonTX 77030USA lester and sue smith breast center Baylor College of MedicineHoustonTX 77030USA Departments of Medicine and Molecular and Cellular Biology Baylor College of MedicineHoustonTX 77030USA

Endocrine therapy is essential for the treatment of patients with estrogen receptor positive (ER+) breast cancer, however, resistance and the development of metastatic disease is common. Understanding how ER+ breast cancer metastasizes is critical since the major cause of death in breast cancer is metastasis to distant organs. Results from many studies suggest dysregulation of the estrogen receptor alpha gene (ESR1) contributes to therapeutic resistance and metastatic biology. This review covers both pre-clinical and clinical evidence on the spectrum ofESR1 alterations including amplification, point mutations, and genomic rearrangement events driving treatment resistance and metastatic potential of ER+ breast cancer. Importantly, we describe how these ESR1 alterations may provide therapeutic opportunities to improve outcomes in patients with lethal, metastatic breast cancer.

关键词： Endocrine therapy resistance ESR1 fusions ESR1 mutations breast cancer metastasis

Microbial communities biostimulated by ethanol during uranium （VI） bioremediation in contaminated sediment as shown by stable isotope probing

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Frontiers of Environmental Science & Engineering 2015年第3期9卷 453-464页

作者： Mary Beth LEIGH Wei-Min WU Erick CARDENAS Ondrej UHLIK sue CARROLL Terry GENTRY Terence L. MARSH Jizhong ZHOU Philip JARDINE Craig S. CRIDDLE James M. TIEDJE center for Microbial Ecology Michigan State University East Lansing MI 48824 USA Institute of Arctic Biology University of Alaska Fairbanks Fairbanks AK 99775 USA Department of Civil and Environmental Engineering Center for Sustainable Development & Global Competitiveness Codiga Resource Recovery Center Stanford University Stanford CA 94305-4020 USA Department of Biochemistry and Microbiology Institute of Chemical Technology Prague Technicka 3 166 28 Prague Czech Republic Environmental Sciences Division Oak Ridge National Laboratory Oak Ridge TN 37831 USA Department of Botany and Microbiology University of Oklahoma Norman OK 73019 USA Department of Crop and Soil Sciences Texas A&M University College Station TX 77843 USA

Stable isotope probing （SIP） was used to identify microbes stimulated by ethanol addition in microcosms containing two sediments collected from the bioremediation test zone at the US Department of Energy Oak Ridge site, TN, USA. One sample was highly bioreduced with ethanol while another was less reduced. Microcosms with the respective sediments were amended with ^13C labeled ethanol and incubated for 7 days for SIP. Ethanol was rapidly converted to acetate within 24h accompanied with the reduction of nitrate and sulfate. The accumulation of acetate persisted beyond the 7 d period. Aqueous U did not decline in the microcosm with the reduced sediment due to desorption of U but continuously declined in the less reduced sample. Microbial growth and concomitant 13C-DNA production was detected when ethanol was exhausted and abundant acetate had accumulated in both microcosms. This coincided with U（VI） reduction in the less reduced sample. I3C originating from ethanol was ultimately utilized for growth, either directly or indirectly, by the dominant microbial community members within 7 days of incubation. The microbial community was comprised predominantly of known denitrifiers, sulfate-reducing bacteria and iron （Ⅲ） reducing bacteria including Desulfovibrio, Sphingomonas, Ferribacterium, Rhodanobacter, Geothrix, Thiobacillus and others, including the known U（VI）-redueing bacteria Acidovorax, Anaeromyxobacter, Desulfovibrio, Geobac- ter and Desulfosporosinus. The findings suggest that ethanol biostimulates the U（VI）-reducing microbial com- munity by first serving as an electron donor for nitrate, sulfate, iron （IH） and U（VI） reduction, and acetate which then functions as electron donor for U（VI） reduction and carbon source for microbial growth.

关键词： Stable isotope probing （S/P） ethanol acetate uranium reduction sediment bioremediation