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Metabolic cell death in cancer:ferroptosis,cuproptosis,disulfidptosis,and beyond

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Protein & Cell 2024年第9期15卷 642-660页

作者： Chao Mao Min Wang Li Zhuang Boyi Gan Department of Experimental Radiation oncology The University of Texas MD Anderson Cancer CenterHoustonTX 77030USA Department of Molecular and Cellular Biology Baylor College of MedicineHoustonTX 77030USA The University of texas MD Anderson UTHealth Graduate School of Biomedical Sciences HoustonTX 77030USA

Cell death resistance represents a hallmark of *** studies have identified metabolic cell death as unique forms of regulated cell death resulting from an imbalance in the cellular *** review discusses the mechanisms of metabolic cell death—ferroptosis,cuproptosis,disulfidptosis,lysozincrosis,and alkaliptosis—and explores their potential in cancer *** review underscores the complexity of the metabolic cell death pathways and offers insights into innovative therapeutic avenues for cancer treatment.

关键词： cell death cancer treatment ferroptosis cuproptosis disulfidptosis

Integrative genomic and transcriptomic profiling of pulmonary sarcomatoid carcinoma identifies molecular subtypes associated with distinct immune features and clinical outcomes

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Cancer Innovation 2024年第3期3卷 81-94页

作者： Sahil Seth Runzhe Chen Yang Liu Junya Fujimoto Lingzhi Hong Alexandre Reuben Susan Varghese Carmen Behrens Tina McDowell Luisa Solis Soto Cara Haymaker Annikka Weissferdt Neda Kalhor Jia Wu Xiuning Le Natalie I Vokes Chao Cheng John V.Heymach Don L.Gibbons P.Andrew Futreal Ignacio IWistuba Humam Kadara Jianhua Zhang Cesar Moran Jianjun Zhang Department of Genomic Medicine The University of Texas MD Anderson Cancer CenterHoustonTexasUSA TRACTION The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Graduate School of Biomedical Sciences The University of Texas MD Anderson and the University of Texas Health Science CenterHoustonTexasUSA Department of Thoracic/Head and Neck Medical oncology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Translational Molecular Pathology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Epidemiology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Pathology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Imaging Physics The University of Texas MD Anderson Cancer CenterHoustonTexasUSA Department of Medicine Baylor College of MedicineHoustonTexasUSA

Background:Pulmonary sarcomatoid carcinoma(PSC)is a rare and aggressive subtype of non-small cell lung cancer(NSCLC),characterized by the presence of epithelial and sarcoma-like *** molecular and immune landscape of PSC has not been well ***:Multiomics profiling of 21 pairs of PSCs with matched normal lung tissues was performed through targeted high-depth DNA panel,whole-exome,and RNA *** describe molecular and immune features that define subgroups of PSC with disparate genomic and immunogenic features as well as distinct clinical ***:In total,27 canonical cancer gene mutations were identified,with TP53 the most frequently mutated gene,followed by ***,most TP53 and KRAS mutations were earlier genomic events mapped to the trunks of the tumors,suggesting branching evolution in most PSC *** identified two distinct molecular subtypes of PSC,driven primarily by immune infiltration and *** Immune High(IM-H)subtype was associated with superior survival,highlighting the impact of immune infiltration on the biological and clinical features of localized ***:We provided detailed insight into the mutational landscape of PSC and identified two molecular subtypes associated with ***-H tumors were associated with favorable recurrence-free survival and overall survival,highlighting the importance of tumor immune infiltration in the biological and clinical features of PSCs.

关键词： genomic immune pulmonary sarcomatoid carcinoma survival

Astrocytic calcium waves:unveiling their roles in sleep and arousal modulation

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Neural Regeneration Research 2024年第5期19卷 984-987页

作者： Erxi Wu Dan Qi Damir Nizamutdinov Jason H.Huang Department of Neurosurgery and Neuroscience Institute Baylor Scott&White HealthTempleTXUSA texas A&M University School of Medicine TempleTXUSA texas A&M University School of Pharmacy College StationTXUSA LIVESTRONG Cancer Institutes and Department of oncology Dell Medical Schoolthe University of Texas at AustinAustinTXUSA Department of Neurosurgery Baylor College of MedicineTempleTXUSA

Neuron-astrocyte interactions are vital for the brain’s *** astrocyte activities is crucial for comprehending the complex neural network,particularly the population-level functions of neurons in different cortical states and associated behaviors in *** on animal sleep and wakefulness have revealed distinct cortical synchrony patterns between ***,outnumbering neurons by nearly fivefold,support and regulate neuronal and synaptic *** research on astrocyte activation during cortical state transitions has emphasized the influence of norepinephrine as a neurotransmitter and calcium waves as key components of ion channel *** summary focuses on a few recent studies investigating astrocyte-neuron interactions in mouse models during sleep,wakefulness,and arousal levels,exploring the involvement of noradrenaline signaling,ion channels,and glutamatergic signaling in different cortical *** findings highlight the significant impact of astrocytes on large-scale neuronal networks,influencing brain activity and *** astrocytic signaling pathways shows promise for treating sleep disorders and arousal *** research is needed to understand astrocytic calcium signaling in different brain regions and its implications for dysregulated brain states,requiring future human studies to comprehensively investigate neuron-astrocyte interactions and pave the way for therapeutic interventions in sleep-and arousal-related disorders.

关键词： arousal astrocyte calcium waves locus coeruleus neuron-astrocyte interaction norepinephrine sleep wakefulness

Proteomic analysis of ferroptosis pathways reveals a role of CEPT1 in suppressing ferroptosis

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Protein & Cell 2024年第9期15卷 686-703页

作者： Xiaoguang Liu Zhen Chen Yuelong Yan Fereshteh Zandkarimi Litong Nie Qidong Li Amber Horbath Kellen Olszewski Lavanya Kondiparthi Chao Mao Hyemin Lee Li Zhuang Masha Poyurovsky Brent RStockwell Junjie Chen Boyi Gan Department of Experimental Radiation oncology The University of Texas MD Anderson Cancer CenterHoustonTX 77030USA Department of Biological Sciences and Department of Chemistry Columbia UniversityNew YorkNY 10027USA Kadmon Corporation LLC(A Sanofi Company)New YorkNY 10016USA The University of texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences HoustonTX 77030USA The Barer Institute PhiladelphiaPA 19104USA

Ferroptosis has been recognized as a unique cell death modality driven by excessive lipid peroxidation and unbalanced cellular *** this study,we established a protein interaction landscape for ferroptosis pathways through proteomic analyses,and identified choline/ethanolamine phosphotransferase 1(CEPT1)as a lysophosphatidylcholine acyltransferase 3(LPCAT3)-interacting protein that regulates LPCAT3 protein *** contrast to its known role in promoting phospholipid synthesis,we showed that CEPT1 suppresses ferroptosis potentially by interacting with phospholipases and breaking down certain pro-ferroptotic polyunsaturated fatty acid(PUFA)-containing ***,our study reveals a previously unrecognized role of CEPT1 in suppressing ferroptosis.

关键词： proteomics ferroptosis CEPT1 LPCAT3

Dual-Fields Rotational Total Skin Electron Therapy: Investigation and Implementation

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International Journal of Medical Physics, Clinical Engineering and Radiation oncology 2024年第1期13卷 1-15页

作者： M. Ming Xu Iris Rusu Richard P. Garza Northwestern Medicine Cancer Center Warrenville and Geneva Illinois USA Department of Radiation oncology Loyola University Medical Center Maywood Illinois USA The Austin Center for Radiation oncology Austin Texas USA

Purpose: To present a protocol of a dual-field rotational (DFR) total skin electron therapy (TSET) and to provide an assessment of clinical implementation, dosimetry properties, and skin dose evaluation. Methods and Materials: The DFR-TSET combined the Stanford 6-field and McGill rotational methods. Dual 6 MeV electron beams in high dose total skin electron mode were used for DFR-TSET on a commercial linac. Beam profiles and dosimetric properties were measured using solid phantoms. The dose rate at expanded source-to-surface distance (SSD) was a combination of static rate and rotational rate. In vivo dosimetry of patient skin was performed on patients’ skin using film, metal oxide semiconductor field-effect transistors (MOSFET), and optically stimulated luminescent dosimeters (OSLD). Results: Dual field rotational total skin electron therapy exhibited good (≤±10%) uniformity in the beam profiles in the vertical direction at an extended SSD of 332 cm with a gantry angulation of ±20˚ deviated from the horizontal direction. In-vivo measurements confirmed acceptable uniformity of the patients’ total body surfaces and revealed anatomically self-blocked or shielded areas where underdosing occurred. Conclusions: The clinical implementation of DFR-TSET effectively utilizes the special mode on a linac. This technique provides short beam-on times, uniform dose distribution, large treatment field, and reduced dose of x-ray contamination to the patients. In-vivo measurements indicate satisfactory delivery and dose uniformity of the prescribed dose. Electron boost fields are recommended at normal SSDs to address underdosed areas.

关键词： Total Skin Electron Therapy Stanford 6 Field McGill Rotation Therapy In-Vivo Dosimetry

Galectin 3-binding protein(LGALS3BP)depletion attenuates hepatic fibrosis by reducing transforming growth factor-β1(TGF-β1)availability and inhibits hepatocarcinogenesis

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Cancer Communications 2024年第10期44卷 1106-1129页

作者： Dae-Hwan Kim Minjeong Sung Myong-Suk Park Eun-Gene Sun Sumin Yoon Kyung Hyun Yoo Kamalakannan Radhakrishnan Sung Yun Jung Woo-Kyun Bae Sang-Hee Cho Ik-Joo Chung Department of Internal Medicine Division of Hematology and OncologyChonnam National University Medical SchoolHwasunSouth Korea Department of Internal Medicine Division of Hematology and OncologyChonnam National University Hwasun HospitalHwasunSouth Korea Combinatorial Tumor Immunotherapy MRC Center Chonnam National University Medical SchoolHwasunSouth Korea National Immunotherapy Innovation Center HwasunSouth Korea BioMedical Sciences Graduate Program Chonnam National UniversityHwasunSouth Korea Department of Biological Science SookmyungWomen’s UniversitySeoulSouth Korea Clinical Vaccine R&D Center Chonnam National UniversityHwasunSouth Korea Department of Biochemistry and Molecular Pharmacology Baylor College of MedicineHoustonTexasUSA

Background:Increased Galectin 3-binding protein(LGALS3BP)serum levels have been used to assess hepatic fibrosis stages and the severity of hepatocellular carcinoma(HCC).Considering the crucial role of transforming growth factor-β1(TGF-β1)in the emergence of these diseases,the present study tested the hypothesis that LGALS3BP regulates the TGF-β1 signaling ***:The expression levels of LGALS3BP and TGFB1 were analyzed in patients with metabolic dysfunction-associated steatohepatitis(MASH)and *** omics techniques,such as RNA-sequencing,transposaseaccessible chromatin-sequencing assay,and liquid chromatography-tandem mass spectrometry proteomics,were used to identify the regulatory mechanisms for the LGALS3BP-TGF-β1 *** effects of altered TGF-β1 signaling by LGALS3BP were investigated in conditional LGALS3BP-knockin and LGALS3BP-knockout ***:In patients with MASH and HCC,the levels of LGALS3BP and TGFB1 exhibited positive *** of LGALS3BP by the inflammatory cytokine interferonαin HCC cells or ectopic overexpression of LGALS3BP in hepatocytes promoted the expression levels of *** fibrosis was observed in the livers of hepatocyte-specific LGALS3BP-knockin mice,with increased TGFB1 ***3BP directly bound to and assembled integrinαV,an integral mediator required for releasing active TGF-β1 from extracellular latent complex with the rearranged F-actin *** released TGF-β1 activated JunB transcription factor,which in turn promoted the TGF-β1 positive feedback ***3BP deletion in the hepatocytes downregulated TGF-β1 signaling and CCl4 induced ***,LGALS3BP depletion hindered hepatocarcinogenesis by limiting the availability of fibrogenic TGF-β***:LGALS3BP plays a crucial role in hepatic fibrosis and carcinogenesis by controlling the TGF-β1 signaling pathway,making it a promising therapeutic target in TGF-β1-related diseases.

关键词： F-actin FAK hepatic carcinogenesis IntegrinαV Interferonα JunB LGALS3BP metabolic dysfuntion-associated steatohepatitis tensile force TGF-β1

Medical management of gastric cancer:A 2014 update

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World Journal of Gastroenterology 2014年第38期20卷 13637-13647页

作者： Elena Elimova Hironori Shiozaki Roopma Wadhwa Kazuki Sudo Qiongrong Chen Jeannelyn S Estrella Mariela A Blum Brian Badgwell Prajnan Das Shumei Song Jaffer A Ajani Department of Gastrointestinal Medical oncology University of TexasAnderson Cancer Center Pathology University of TexasAnderson Cancer Center Surgical oncology University of TexasAnderson Cancer Center Radiation oncology University of TexasAnderson Cancer Center

Gastric cancer represents a serious health problem on a global scale. It is the second leading cause of cancer-related death worldwide. Novel therapeutic targets are desperately needed because the meager improvement in the cure rate of about 10% realized by adjunctive treatments to surgery is unacceptable as > 50% patients with localized gastric cancer succumb to their disease. Either postoperative chemoradiotherapy (United States), pre-and post-operative chemotherapy (Europe), and adjuvant chemotherapy after a D2 resection (Asia) can all be regarded as standards of care in the localized gastric cancer management. In metastatic disease the addition of trastuzumab to chemotherapy is standard of care in Her2 positive disease. In the HER2 negative population, the treatments remain limited. In the first line setting, the standard of care is a combination of fluoropyrimidine and platinum containing chemotherapy, with or without epirubicin or docetaxel. The results of targeted therapy trials have by and large been disappointing, but none of these trials looked at an appropriately enriched population. Finally there is a meager overall survival benefit in treating patients with metastatic disease in the second line setting, with either irinotecan, docetaxel or ramucirumab however none of these drugs have been compared head to head in a well-powered randomized controlled trial.

关键词： Chemotherapy Gastric cancer Chemoradiation Metastatic Localized

Overcoming EGFR-TKI resistance by targeting the tumor microenvironment

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Chinese Medical Journal Pulmonary and Critical Care Medicine 2024年第3期2卷 151-161页

作者： Jinsong Zhang Natalie Vokes Man Li Jiachen Xu Hua Bai Jie Wang Zhijie Wang Jianjun Zhang State Key Laboratory of Molecular oncology CAMS Key Laboratory of Translational Research on Lung CancerDepartment of Medical OncologyNational Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeNo.17PanjiayuannanliChaoyang DistrictBeijing 100021China Department of Thoracic/Head and Neck Medical oncology Department of Genomic MedicineThe Lung Cancer Interception ProgramThe Lung Cancer Genomics ProgramThe University of TexasMD Anderson Cancer CenterHoustonTX 77030USA Shanxi Cancer Hospital(Shanxi Cancer Institute) Cancer Hospital of Chinese Academy of Medical Sciences Shanxi HospitalShanxi Medical University Affiliated HospitalTaiyuanShanxi 030013China

Targeted therapy has ushered in a new era of precision medicine for non-small cell lung cancer(NSCLC).Currently,epidermal growth factor receptor(EGFR)-tyrosine kinase inhibitors(TKIs)stand as the recommended first-line therapy for advanced NSCLC harboring sensitive EGFR ***,most patients inevitably confront the challenge of drug *** phenomenon arises not solely from intrinsic alterations within cancer cells but also from the intricate dynamics of the tumor microenvironment and the complex interactions that occur between cancer cells and their immediate *** review consolidates the current knowledge regarding EGFR-TKI resistance mechanisms,with a specific emphasis on unraveling the role played by the tumor *** addition,the review delineates strategic approaches to surmount TKI resistance,thereby enriching the understanding of the interplay between therapeutic agents and the intricate milieu surrounding cancer cells.

关键词： Non-small cell lung cancer Epidermal growth factor receptor Tumor microenvironment Epidermal growth factor receptor-tyrosine kinase inhibitor Drug resistance

Regulation of tumor cell migration by protein tyrosine phosphatase (PTP)-proline-, glutamate-, serine-,and threonine-rich sequence(PEST)

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Chinese Journal of Cancer 2013年第2期32卷 75-83页

作者： Yanhua Zheng Zhimin Lu Brain Tumor Center and Department of Neuro-oncology The University of Texas MD Anderson Cancer Center Department of Molecular and Cellular oncology The University of Texas MD Anderson Cancer Center The University of texas Graduate School of Biomedical Sciences at Houston

Protein tyrosine phosphatase (PTP)-proline-,glutamate-,serine-,and threonine-rich sequence (PEST) is ubiquitously expressed and is a critical regulator of cell adhesion and ***-PEST activity can be regulated transcriptionally via gene deletion or mutation in several types of human cancers or via post-translational modifications,including phosphorylation,oxidation,and caspase-dependent ***-PEST interacts with and dephosphorylates cytoskeletal and focal adhesion-associated ***-phorylation of PTP-PEST substrates regulates their enzymatic activities and/or their interaction with other proteins and plays an essential role in the tumor cell migration process.

关键词：蛋白酪氨酸磷酸酶细胞迁移 PEST 肿瘤细胞脯氨酸 PTP 谷氨酸丝氨酸