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Rezatapopt (PC14586): A First-in-Class Small Molecule p53 Y220C Mutant Protein Stabilizer in Clinical Trials

JOURNAL OF MEDICINAL CHEMISTRY 2025年第7期68卷 6847-6849页

作者： Ma, Zonghui Shen, Qiang Zhou, Jia Chemical Biology Program Department of Pharmacology and Toxicology University of Texas Medical Branch (UTMB) Galveston Texas 77555 United States Department of Interdisciplinary Oncology School of Medicine LSU LCMC Health Cancer Center Louisiana State University Health Sciences Center New Orleans Louisiana 70112 United States

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Biomedical data and AI

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Science China Life Sciences 2025年第5期68卷 1536-1540页

作者： Hao Xu Shibo Zhou Zefeng Zhu Vincenzo Vitelli Liangyi Chen Ziwei Dai Ning Yang Luhua Lai Shengyong Yang Sergey Ovchinnikov Zhuoran Qiao Sirui Liu Chen Song Jianfeng Pei Han Wen Jianfeng Feng Yaoyao Zhang Zhengwei Xie Yang-Yu Liu Zhiyuan Li Fulai Jin Hao Li Mohammad Lotfollahi Xuegong Zhang Ge Yang Shihua Zhang Ge Gao Pulin Li Qi Liu Jing-Dong Jackie Han Peking-Tsinghua Center for Life Sciences (CLS) Academy for Advanced Interdisciplinary StudiesPeking University Center for Quantitative Biology (CQB) Academy for Advanced Interdisciplinary StudiesPeking University Peking University-Tsinghua University-National Institute of Biological Sciences Joint Graduate Program Academy for Advanced Interdisciplinary StudiesPeking University Department of Physics University of Chicago School of Life Sciences Southern University of Science and Technology Peking University Chengdu Academy for Advanced Interdisciplinary Biotechnologies College of Chemistry and Molecular Engineering Peking University Department of Biotherapy Cancer Center and State Key Laboratory of BiotherapyWest China HospitalSichuan University Department of Biology Massachusetts Institute of Technology Lambic Therapeutics Inc. Changping Laboratory Al for Science Institute Key Laboratory of Computational Neuroscience and Brain-Inspired Intelligence Fudan University Department of Obstetrics and Gynecology West China Second University HospitalSichuan University Peking University International Cancer Institute and Peking University-Yunnan Baiyao International Medical Institute and State Key Laboratory of Natural and Biomimetic Drugs Department of Molecular and Cellular PharmacologySchool of Pharmaceutical SciencesPeking University Health Science CenterPeking University Channing Division of Network Medicine Department of MedicineBrigham and Women's Hospital and Harvard Medical School Center for Artificial Intelligence and Modeling the Carl R.Woese Institute for Genomic BiologyUniversity of Illinois Urbana-Champaign Department of Genetics and Genome Sciences School of Medicine and Department of Computer and Data Sciences and Department of Population and Quantitative Health SciencesCase Western Reserve University Department of Biochemistry and Biophysics University of California Sanger Institute Department of Automation Tsinghua University State Key Laboratory of Multimodal Artificial Intelligence Systems I

The development of artificial intelligence(AI) and the mining of biomedical data complement each other. From the direct use of computer vision results to analyze medical images for disease screening, to now integrating biological knowledge into models and even accelerating the development of new AI based on biological discoveries, the boundaries of both are constantly expanding, and their connections are becoming closer.

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Scaling Up Synthetic Cell Production Using Robotics and Machine Learning Toward Therapeutic Applications

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Advanced biology 2025年第0期 e2400671页

作者： Sharf-Pauker, Noga Galil, Ido Kfir, Omer Chen, Gal Menachem, Rotem Shklover, Jeny Schroeder, Avi Ackerman, Shanny The Louis Family Laboratory for Targeted Drug Delivery and Personalized Medicine Technologies Department of Chemical Engineering Technion – Israel Institute of Technology Haifa32000 Israel The Norman Seiden Multidisciplinary Program for Nanoscience and Nanotechnology Technion – Israel Institute of Technology Haifa32000 Israel Faculty of Computer Science Technion – Israel Institute of Technology Haifa32000 Israel The Interdisciplinary Program for Biotechnology Technion – Israel Institute of Technology Haifa32000 Israel Cell Biology and Cancer Science Rappaport Faculty of Medicine Technion – Israel Institute of Technology Haifa32000 Israel

Synthetic cells (SCs), developed through bottom-up synthetic biology, hold great potential for biomedical applications, with the promise of replacing malfunctioning natural cells and treating diseases with spatiotemporal control. Currently, most SC synthesis and characterization processes are manual, limiting scalability and efficiency. In this study, an automated method is developed for large-scale production of protein-producing SCs for therapeutic applications. The optimized process, compatible with a robotic liquid handling system (LiHa), reduces production time by half. Additionally, incorporation of an automated tissue dissociator-based emulsification increases batch size 30-fold while preserving SC characteristics. To assess SC quality and protein synthesis, artificial intelligence (AI)-based image analysis is employed, allowing for automated, accurate and high-throughput SC characterization. Large-scale luciferase-expressing SCs from a single homogeneous batch are administered to mice, allowing for real-time monitoring of protein expression and reducing experimental variability. By troubleshooting several central steps in SC synthesis, it is demonstrated that automation and computerized quality control can significantly improve the process of SC synthesis for preclinical and clinical applications. © 2025 The Author(s). Advanced biology published by Wiley-VCH GmbH.

关键词： AI artificial Intelligence automation machine learning robotics synthetic biology synthetic cells

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Building (Viral) Phylogenetic Trees Using a Maximum Likelihood Approach

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Current Protocols in Microbiology 2018年第1期51卷 e63/1-e63/24页

作者： King, Kelly M. Van Doorslaer, Koenraad School of Animal and Comparative Biomedical Sciences University of Arizona Tucson AZ United States Department of Immunobiology Cancer Biology Graduate Interdisciplinary Program Genetics Graduate Interdisciplinary Program BIO5 Institute and the University of Arizona Cancer Center University of Arizona Tucson AZ United States

Phylogenetic analyses allow for inferring a hypothesis about the evolutionary history of a set of homologous molecular sequences. This hypothesis can be used as the basis for further molecular and computational studies. In this unit, we offer one specific method to construct a Maximum Likelihood phylogenetic tree. We outline how to identify homologous sequences and construct a multiple sequence alignment. Following alignment, sequences are screened for potentially confounding factors such as recombination and genetic saturation. Finally, a Maximum Likelihood phylogenetic tree can be constructed implementing a rigorously tested model of evolution. The workflow outlined in this unit provides sufficient background for inferring a robust phylogenetic tree starting from a particular gene of interest. © 2018 by John Wiley & Sons, Inc. © 2018 John Wiley & Sons, Inc.

关键词： evolution maximum likelihood phylogeny saturation virus

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Correction: AR loss in prostate cancer stroma mediated by NF-κB and p38-MAPK signaling disrupts stromal morphogen production

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Oncogene 2025年第1期44卷 50页

作者： Shekha Tahsin Neha S Sane Brent Cernyar Linan Jiang Yitshak Zohar Benjamin R Lee Cindy K Miranti Cancer Biology Graduate Interdisciplinary Program University of Arizona Tucson AZ USA. Department of Cellular and Molecular Medicine University of Arizona Tucson AZ USA. Department of Aerospace and Mechanical Engineering University of Arizona Tucson AZ USA. University of Arizona Cancer Center University of Arizona Tucson AZ USA. Department of Urology University of Arizona Tucson AZ USA. Cancer Biology Graduate Interdisciplinary Program University of Arizona Tucson AZ USA. cmiranti@arizona.edu. Department of Cellular and Molecular Medicine University of Arizona Tucson AZ USA. cmiranti@arizona.edu. University of Arizona Cancer Center University of Arizona Tucson AZ USA. cmiranti@arizona.edu.

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Multiplex gene editing models of del(7q) reveal combined CUX1 and EZH2 loss drives clonal expansion and drug resistance

Blood Neoplasia

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Blood Neoplasia 2025年第2期2卷 100083-100083页

作者： Matthew R. M. Jotte Angela Stoddart Tanner C. Martinez Raven Moten Yuqing Xue Molly K. Imgruet Hunter Blaylock Henna S. Nam Bonnie Hu Jermaine Austin Ningfei An Saira Khan Sandeep K. Gurbuxani Megan E. McNerney Interdisciplinary Scientist Training Program The University of Chicago Medicine Chicago IL Department of Pathology The University of Chicago Medicine Chicago IL Committee on Cancer Biology The University of Chicago Medicine Chicago IL Department of Pediatrics The University of Chicago Medicine Chicago IL Committee on Immunology The University of Chicago Medicine Chicago IL Committee on Genetics Genomics and Systems Biology The University of Chicago Medicine Chicago IL The University of Chicago Medicine Comprehensive Cancer Center The University of Chicago Medicine Chicago IL

Abstract Loss of all or part of chromosome 7 [−7/del(7q)] is recurrent in myeloid neoplasms and associated with a poor response to chemotherapy. Chromosome 7–encoded genes driving drug resistance and the consequences of combinatorial 7q tumor suppressor gene loss have remained unclear, the latter question largely because of the challenges of modeling aneuploidy. Here, we use in silico data mining to uncover 7q genes involved in chemotherapy resistance. We establish murine models of del(7q) clonal hematopoiesis and drug resistance with multiplex CRISPR-Cas9 (CRISPR–associated protein 9)–mediated inactivation of 4 genes, Cux1 , Ezh2 , Kmt2c , and Kmt2e . Postgenotoxic exposure, combined deficiency of Cux1 and Ezh2 preferentially promotes clonal myeloid expansion in vivo, with compounding defects in DNA damage recognition and repair. Human acute myeloid leukemia cell lines similarly illustrate central roles for CUX1 and EZH2 loss in survival and DNA damage resolution after chemotherapy exposure. Transcriptome analysis reveals combined Cux1 and Ezh2 loss recapitulates gene signatures of -7 patients and defective DNA damage response pathways, to a greater extent than single gene loss. This work reveals a genetic interaction between CUX1 and EZH2 , and sheds light on how −7/del(7q) contributes to leukemogenesis and drug resistance characteristic of these adverse-risk neoplasms. These data support the concept of 7q as a contiguous gene syndrome region, in which combined loss of multiple gene drives pathogenesis. Furthermore, our CRISPR-based approach may serve as a framework for interrogating other recurrent aneuploid events in cancer.

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Substituents introduction of methyl and methoxy functional groups on resveratrol stabilizes mTOR binding for autophagic cell death induction

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Scientific Reports 2025年第1期15卷 1-27页

作者： Ei, Zin Zin Racha, Satapat Chunhacha, Preedakorn Yokoya, Masashi Moriue, Sohsuke Zou, Hongbin Chanvorachote, Pithi Department of Pharmacology and Physiology Faculty of Pharmaceutical Sciences Chulalongkorn university Bangkok 10330 Thailand Center of Excellence in Cancer Cell and Molecular Biology Faculty of Pharmaceutical Sciences Chulalongkorn University Bangkok 10330 Thailand Faculty of Pharmacy Silpakorn University Nakhon Pathom Thailand Sustainable Environment Research Institute Chulalongkorn University Bangkok Thailand Interdisciplinary Program in Pharmacology Graduate School Chulalongkorn university Bangkok 10330 Thailand Department of Biochemistry and Microbiology Faculty of Pharmaceutical Sciences Chulalongkorn University Bangkok Thailand Department of Pharmaceutical Chemistry Meiji Pharmaceutical University 2-522-1 Noshio Kiyose Tokyo 204-8588 Japan College of Pharmaceutical Sciences Zhejiang University Hangzhou 310058 China

The regulation of the mammalian target of rapamycin (mTOR) protein by cancer cells can lead to uncontrol of cancer cell growth and cancer therapy resistance. The drug discovery of the anticancer agent 5-(3-hydroxy-4-methoxyphenethyl)-2-methoxy-3-methylphenol (SM-3), a derivative of resveratrol by substituting a methyl group at the hydroxy group of ring A and adding a methoxy group at the para position of ring B, shows promising potential for targeting autophagy to induce cell death and suppress cancer stem cells (CSCs) through the inhibition of the mTOR protein. In human lung cancer cells, SM-3 showed greater efficacy, with lower IC₅₀ values of 72.74 ± 0.13, 67.66 ± 0.10, and 43.24 ± 0.11 µM in A549, H292, and H460 cells, respectively, compared to the parent compound, Resveratrol (Res). Moreover, the selectivity index (SI) values for BEAS2B cells compared to tumor cells treated with SM-3 were 10.99, 11.81, and 18.49 for A549, H292, and H460 cell lines, respectively. Therefore, SM-3 treatment led to reduced proliferation rates and colony formation in lung cancer cells. In our study, spheroids treated with SM-3 showed a higher proportion of dead spheroids compared to those treated with Res. Additionally, SM-3 treatment resulted in decreased expression of stem cell markers (CD133, CD44, and ALDH1A1) and transcription factors (OCT4, NANOG, and SOX2) in spheroids and organoids from human lung cancer cells by inhibiting the mTOR/pAkt pathway. SM-3 was also found to induce autophagic cell death, as indicated by Monodansylcadaverine staining, acidic vesicle formation, and the conversion of LC3BI to LC3BII. Using MM/GBSA calculations, SM-3 exhibited a stronger binding affinity (-25.09 kcal/mol) compared to Res (-18.85 kcal/mol). SM-3 also displayed greater stability during the entire simulation, maintaining lower RMSD values of 2–3 Å even after 80 ns. In summary, the introduction of methyl and methoxy functional groups on Res to create SM-3 effectively suppressed

关键词： Autophagy Lung cancer mTOR Resveratrol SM-3 Stem cells

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Osteolytic effects of tumoral estrogen signaling in an estrogen receptor-positive breast cancer bone metastasis model

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Journal of cancer Metastasis and Treatment 2021年第1期7卷 254-271页

作者： Julia N.Cheng Jennifer B.Frye Susan A.Whitman Andrew G.Kunihiro Julia A.Brickey Janet L.Funk Cancer Biology Graduate Interdisciplinary Program University of ArizonaTucsonAZ 85724USA Department of Medicine University of ArizonaTucsonAZ 85724USA Department of Nutritional Sciences University of ArizonaTucsonAZ 85724USA

Aim:Estrogen receptorα-positive(ER+)subtypes of breast cancer have the greatest predilection for forming osteolytic bone metastases(BMETs).Because tumor-derived factors mediate osteolysis,a possible role for tumoral ERαsignaling in driving ER+BMET osteolysis was queried using an estrogen(E2)-dependent ER+breast cancer BMET ***:Female athymic Foxn1nu mice were inoculated with human ER+MCF-7 breast cancer cells via the left cardiac ventricle post-E2 pellet placement,and age-and dose-dependent E2 effects on osteolytic ER+BMET progression,as well as direct bone effects of E2,were ***:Osteolytic BMETs,which did not form in the absence of E2 supplementation,occurred with the same frequency in young(5-week-old)*** mature(16-week-old)E2(0.72 mg)-treated mice,but were larger in young mice where anabolic bone effects of E2 were ***,in mice of a single age and across a range of E2 doses,anabolic E2 bone effects were constant,while osteolytic ER+BMET lesion incidence and size increased in an E2 dose-dependent *** in ER+tumor-bearing(but not tumor-naive)mice increased in an E2-dose dependent fashion at the bone-tumor interface,while histologic tumor size and proliferation did not vary with E2 dose.E2-inducible tumoral secretion of the osteolytic factor parathyroid hormone-related protein(PTHrP)was dose-dependent and mediated by ERα,with significantly greater levels of secretion from ER+BMET-derived tumor ***:These results suggest that tumoral ERαsignaling may contribute to ER+BMET-associated osteolysis,potentially explaining the greater predilection for ER+tumors to form clinically-evident osteolytic BMETs.

关键词： Breast cancer estrogen receptor bone metastasis estradiol osteolysis osteoclasts parathyroid hormone-related protein bone

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S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis

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Bone Research 2019年第4期7卷 424-436页

作者： Haemin Kim Bongjun Kim Sang Il Kim Hyung Joon Kim Brian YRyu Junho Chung Zang Hee Lee Hong-Hee Kim Department of Cell and Developmental Biology BK21 Program and DRISeoul National UniversitySeoulKorea Department of Biochemistry and Molecular Biology Seoul National University College of MedicineSeoulKorea Cancer Research Institute Seoul National University College of MedicineSeoulKorea Department of Cancer Biology Seoul National University College of MedicineSeoulKorea Department of Oral Physiology BK21 PLUS Projectand Dental and Life Science InstituteSchool of DentistryPusan National UniversityYangsanKorea Interdisciplinary Program in Bioinformatics Seoul National University College of Natural SciencesSeoulKorea Department of Biomedical Sciences Seoul National University Graduate SchoolSeoulKorea

Bone destruction induced by breast cancer metastasis causes severe complications,including death,in breast cancer *** between cancer cells and skeletal cells in metastatic bone microenvironments is a principal element that drives tumor progression and ***-derived factors play fundamental roles in this form of *** identify soluble factors released from cancer cells in bone metastasis,we established a highly bone-metastatic subline of MDA-MB-231 breast cancer *** subline(mtMDA)showed a markedly elevated ability to secrete S100A4 protein,which directly stimulated osteoclast formation via surface receptor *** S100A4 stimulated osteoclastogenesis in vitro and bone loss in *** medium from mtMDA cells in which S100A4 was knocked down had a reduced ability to stimulate ***,the S100A4 knockdown cells elicited less bone destruction in mice than the control knockdown *** addition,administration of an anti-S100A4 monoclonal antibody(mAb)that we developed attenuated the stimulation of osteoclastogenesis and bone loss by mtMDA in *** together,our results suggest that S100A4 released from breast cancer cells is an important player in the osteolysis caused by breast cancer bone metastasis.

关键词： S100A4 breast metastatic

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In vivo validation of metastasis-regulating microRNA-766 in human triple-negative breast cancer cells

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Laboratory Animal Research 2017年第3期33卷 256-263页

作者： Oh, Keunhee Lee, Dong-Sup Laboratory of Immunology/Cancer Biology Department of Biomedical Sciences Seoul National University College of Medicine 103 Daehakro Jongno-gu Seoul 03080 South Korea Cancer Research Institute Interdisciplinary Program of Tumor Biology Seoul National University College of Medicine Seoul South Korea Transplantation Research Institute Seoul National University College of Medicine Seoul South Korea

Breast cancer is the second most common cancer and the most frequent cancer in women worldwide. Recent improvements in early detection and effective adjuvant chemotherapies have improved the survival of breast cancer patients. Even with initial disease remission, one-third of all breast cancer patients will relapse with distant metastasis. Breast cancer metastasis is largely an incurable disease and the main cause of death among breast cancer patients. cancer metastasis is comprised of complex processes that are usually not controllable by intervention of a single molecular target. As a single microRNA (miRNA) can affect the aggressiveness of breast cancer cells by concurrently modulating multiple pathway effectors, a metastasis-regulating miRNA would represent a good disease target candidate. In this study, we evaluated the functional capacity of a newly defined human metastasis-related miRNA, miR-766, which was previously identified by comparing a patient-derived xenograft primary tumor model and a metastasis model. Compared to vector-transfected control cells, miR-766-overexpressed triple-negative breast cancer cells exhibited similar primary tumor growth in the orthotopic xenograft model. In contrast, tumor sphere formation and Matrigel invasion were significantly decreased in miR-766-overexpressed breast cancer cells compared with control cancer cells. In addition, lung metastasis was dramatically reduced in miR-766-overexpressed breast cancer cells compared with control cells. Thus, miR-766 affected the distant metastasis process to a greater extent than cancer cell proliferation and primary tumor growth, and may represent a future therapeutic target to effectively control fatal breast cancer metastasis. © 2017, BioMed Central Ltd.

关键词： Human triple-negative breast cancer metastasis microRNA

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