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Understanding the Novel Approach of Nanoferroptosis for Cancer Therapy

Nano-Micro Letters 2024年第9期16卷 501-556页

作者： Afsana Sheikh Prashant Kesharwani Waleed H.Almalki Salem Salman Almujri Linxin Dai zhe‑sheng chen Amirhossein Sahebkar Fei Gao Department of Pharmaceutics School of Pharmaceutical Education and ResearchJamia HamdardNew Delhi 110062India Department of Pharmacology and Toxicology Faculty of PharmacyUmm Al-Qura UniversityMakkahSaudi Arabia Department of Pharmacology College of PharmacyKing Khalid University61421 Asir‑AbhaSaudi Arabia State Key Laboratory of Southwestern Chinese Medicine Resources Pharmacy SchoolChengdu University of Traditional Chinese MedicineChengdu 611130People’s Republic of China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityNew York 11439USA Biotechnology Research Center Pharmaceutical Technology InstituteMashhad University of Medical SciencesMashhadIran Applied Biomedical Research Center Mashhad University of Medical SciencesMashhadIran

As a new form of regulated cell death,ferroptosis has unraveled the unsolicited theory of intrinsic apoptosis resistance by cancer cells.The molecular mechanism of ferroptosis depends on the induction of oxidative stress through excessive reactive oxygen species accumulation and glutathione depletion to damage the structural integrity of cells.Due to their high loading and structural tunability,nanocarriers can escort the delivery of ferro-therapeutics to the desired site through enhanced permeation or retention effect or by active targeting.This review shed light on the necessity of iron in cancer cell growth and the fascinating features of ferroptosis in regulating the cell cycle and metastasis.Additionally,we discussed the effect of ferroptosis-mediated therapy using nanoplatforms and their chemical basis in overcoming the barriers to cancer therapy.

关键词： Ferroptosis Nanoparticles Ferrotherapy Cancer Genes Nanotechnology Toxicity Reactive oxygen species

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Redox signaling-governed drug-tolerant persister cancer cell:a key spark of treatment failure

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Signal Transduction and Targeted Therapy 2022年第4期7卷 955-957页

作者： Liwu Fu zhe-sheng chen State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineGuangdong Esophageal Cancer InstituteCancer CenterSun Yat-Sen UniversityGuangzhou 510060China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA Institute for Biotechnology St.John’s UniversityQueensNY 11439USA

In a recent study published in EMBO Molecular medicine,Zhang et al.provided a novel insight regarding better knowledge of the drug resistant contribution of drug-tolerant persister(DTP)state in tumor evolution,especially in terms of mechanistic insights into redox regulation involved,unambiguously establishing a novel therapeutic strategy of treating multi-drug-resistant(MDR)cancer cells and preventing tumor recurrence by disequilibrating Niemann–Pick C1-like 1(NPC1L1)-mediated redox homeostasis.

关键词： cancer homeostasis insight

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Progress in the studies on the molecular mechanisms associated with multidrug resistance in cancers

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Acta Pharmaceutica Sinica B 2023年第3期13卷 982-997页

作者： Lei Zhang Biwei Ye Zhuo chen zhe-sheng chen State Key Laboratory of Structural Chemistry Fujian Institute of Research on the Structure of MatterChinese Academy of SciencesFuzhou 350002China University of Chinese Academy of Sciences Beijing 100049China Fujian Agriculture and Forestry University Fuzhou 350002China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John's UniversityNew YorkNY 11439USA

Chemotherapy is one of the important methods to treat cancer,and the emergence of multidrug resistance(MDR)is one major cause for the failure of cancer chemotherapy.Almost all anti-tumor drugs develop drug resistance over a period of time of application in cancer patients,reducing their effects on killing cancer cells.Chemoresistance can lead to a rapid recurrence of cancers and ultimately patient death.MDR may be induced by multiple mechanisms,which are associated with a complex process of multiple genes,factors,pathways,and multiple steps,and today the MDR-associated mechanisms are largely unknown.In this paper,from the aspects of protein–protein interactions,alternative splicing(AS)in pre-mRNA,non-coding RNA(ncRNA)mediation,genome mutations,variance in cell functions,and influence from the tumor microenvironment,we summarize the molecular mechanisms associated with MDR in cancers.In the end,prospects for the exploration of antitumor drugs that can reverse MDR are briefly discussed from the angle of drug systems with improved targeting properties,biocompatibility,availability,and other advantages.

关键词： Multidrug resistance(MDR) ABC transporter family Signaling pathway Alternative splicing(AS) Gene mutation None-coding RNA(ncRNA) Tumor microenvironment

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Gut microbes regulate the feeding center:a newdiscovery of Gut Brain Axis

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Signal Transduction and Targeted Therapy 2022年第9期7卷 3168-3169页

作者： Fengwu chen Kajian Hou zhe-sheng chen Department of Endocrinology and metbolic diseases The First Afliated Hospital of Shantou University Medical Collge515000 ShantouGuangdongPR China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John's UniversityNew YorkNY 11439USA

Recently,llana Gabanyi and colleagues published an article in Science,1identifying a microbial sensing mechanism that regulates feeding behavior and host metabolism.In their study,a sex-and age-dependent gut-brain cross-talk is revealed.Their study confrmed that hypothalamic neurons can directly sense the structural components of the gut bacterial microbiota and regulate feeding and nesting behavior,affecting food intake and body temperature.

关键词： temperature. intake feeding

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Tumor cell plasticity in targeted therapy-induced resistance:mechanisms and new strategies

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Signal Transduction and Targeted Therapy 2023年第4期8卷 1503-1523页

作者： zhen-Duo Shi Kun Pang Zhuo-Xun Wu Yang Dong Lin Hao Jia-Xin Qin Wei Wang zhe-sheng chen Cong-Hui Han Department of Urology Xuzhou Clinical School of Xuzhou Medical UniversityJiangsuChina Department of Urology Xuzhou Central HospitalXuzhouJiangsuChina School of Life Sciences Jiangsu Normal UniversityJiangsuChina Department of Urology Heilongjiang Provincial HospitalHeilongjiangChina Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA Department of Medical College Southeast UniversityNanjingChina

Despite the success of targeted therapies in cancer treatment,therapy-induced resistance remains a major obstacle to a completecure.Tumor cells evade treatments and relapse via phenotypic switching driven by intrinsic or induced cell plasticity.Severalreversible mechanisms have been proposed to circumvent tumor cell plasticity,including epigenetic modifications,regulation oftranscription factors,activation or suppression of key signaling pathways,as well as modification of the tumor environment.Epithelial-to-mesenchymal transition,tumor cell and cancer stem cell formation also serve as roads towards tumor cell plasticity.Corresponding treatment strategies have recently been developed that either target plasticity-related mechanisms or employcombination treatments.In this review,we delineate the formation of tumor cell plasticity and its manipulation of tumor evasionfrom targeted therapy.We discuss the non-genetic mechanisms of targeted drug-induced tumor cell plasticity in various types oftumors and provide insights into the contribution of tumor cell plasticity to acquired drug resistance.New therapeutic strategiessuch as inhibition or reversal of tumor cell plasticity are also presented.We also discuss the multitude of clinical trials that areongoing worldwide with the intention of improving clinical outcomes.These advances provide a direction for developing noveltherapeutic strategies and combination therapy regimens that target tumor cell plasticity.

关键词： targeted plasticity resistance

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Microbiota in health and diseases

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Signal Transduction and Targeted Therapy 2022年第5期7卷 1491-1518页

作者： Kaijian Hou Zhuo-Xun Wu Xuan-Yu chen Jing-Quan Wang Dongya Zhang Chuanxing Xiao Dan Zhu Jagadish B.Koya Liuya Wei Jilin Li zhe-sheng chen Department of Endocrine and Metabolic Diseases Longhu HospitalThe First Affiliated Hospital of Medical College of Shantou UniversityShantouGuangdong 515000China Department of Pharmaceutical Sciences Institute for BiotechnologyCollege of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA Microbiome Research Center Moon(Guangzhou)Biotech LtdGuangzhou 510535China School of Pharmacy Weifang Medical UniversityWeifangShandong 261053China Department of Cardiovascular The Second Affiliated Hospital of Medical College of Shantou UniversityShantouGuangdong 515000China

The role of microbiota in health and diseases is being highlighted by numerous studies since its discovery.Depending on the localized regions,microbiota can be classified into gut,oral,respiratory,and skin microbiota.The microbial communities are in symbiosis with the host,contributing to homeostasis and regulating immune function.However,microbiota dysbiosis can lead to dysregulation of bodily functions and diseases including cardiovascular diseases(CVDs),cancers,respiratory diseases.

关键词： diseases respiratory homeostasis

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MET inhibitor tepotinib antagonizes multidrug resistance mediated by ABCG2 transporter:In vitro and in vivo study

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Acta Pharmaceutica Sinica B 2022年第5期12卷 2609-2618页

作者： Zhuo-Xun Wu Qiu-Xu Teng Yuqi Yang Nikita Acharekar Jing-Quan Wang Min He Sabesan Yoganathan Jun Lin Jian Wang zhe-sheng chen Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA Department of Anesthesiology Stony Brook University Health Sciences CenterStony BrookNY 11794USA Department of Radiotherapy the Afﬁliated Jiangyin People’s Hospital of Nantong UniversityJiangyin 214400China

Overexpression of ABCG2 transporter in cancer cells has been linked to the development of multidrug resistance(MDR), an obstacle to cancer therapy. Our recent study uncovered that the MET inhibitor,tepotinib, is a potent reversal agent for ABCB1-mediated MDR. In the present study, we reported for the first time that the MET inhibitor tepotinib can also reverse ABCG2-mediated MDR in vitro and in vivo by directly binding to the drug-binding site of ABCG2 and reversibly inhibiting ABCG2 drug efflux activity, therefore enhancing the cytotoxicity of substrate drugs in drug-resistant cancer cells. Furthermore, the ABCB1/ABCG2 double-transfected cell model and ABCG2 gene knockout cell model demonstrated that tepotinib specifically inhibits the two MDR transporters. In mice bearing drug-resistant tumors, tepotinib increased the intratumoral accumulation of ABCG2 substrate drug topotecan and enhanced its antitumor effect. Therefore, our study provides a new potential of repositioning tepotinib as an ABCG2 inhibitor and combining tepotinib with substrate drugs to antagonize ABCG2-mediated MDR.

关键词： MET inhibitor Tepotinib Multidrug resistance ABCG2 transporter Reversal agent Combination treatment Chemotherapy In vivo study

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Stellettin B renders glioblastoma vulnerable to poly (ADPribose) polymerase inhibitors via suppressing homologydirected repair

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Signal Transduction and Targeted Therapy 2023年第4期8卷 1388-1391页

作者： Xin Peng Yingying Wang Shaolu Zhang zhennan Tao Yuxiang Dai Francois X.Claret Moshe Elkabets Hou-Wen Lin zhe-sheng chen Dexin Kong Tianjin Key Laboratory of Technologies Enabling Development of Clinical Therapeutics and Diagnostics School of PharmacyTianjin Medical UniversityTianjin 300070China Key Laboratory of Immune Microenvironment and Diseases(Ministry of Education) Tianjin Medical UniversityTianjin 300070China Department of Systems Biology The University of Texas MD Anderson Cancer CenterHoustonTX 77030USA Department of Neurosurgery the Affiliated Drum Tower HospitalSchool of MedicineNanjing UniversityNanjing 210008China The Shraga Segal Department of Microbiology Immunology and GeneticsFaculty of Health SciencesBen-Gurion University of the NegevBeer-Sheva 84105Israel Research Center for Marine Drugs State Key Laboratory of Oncogenes and Related GenesDepartment of PharmacyRenji HospitalSchool of MedicineShanghai Jiaotong UniversityShanghai 200127China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA

Dear Editor,Glioblastoma(GBM)is one of the most fatal brain tumors.Current first-line post-surgery regimens for GBM including radiotherapy and temozolomide(TMZ)chemotherapy show very limited efficacy.1,2 Novel therapeutic approaches for GBM patients are urgently needed.Natural products are important sources for drug discovery,especially in the field of cancer treatment.3 We previously isolated stellettin B(STELB)(Fig.1a)from marine sponge(Jaspis stellifera)and reported the remarkable and specific anticancer activities.Recently,a series of stellettins has been totally synthesized and the core chemical structure has been indicated.4 However,the specific mechanism and its role in regulating tumor biology remain largely unknown.

关键词： chemotherapy surgery render

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Detailed resume of RNA m^(6)A demethylases

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Acta Pharmaceutica Sinica B 2022年第5期12卷 2193-2205页

作者： Dandan Shen Bo Wang Ya Gao Lijuan Zhao Yaping Bi Jinge Zhang Ning Wang Huiqin Kang Jingru Pang Ying Liu Luping Pang zhe-sheng chen Yi-Chao zheng Hong-Min Liu Key Laboratory of Advanced Drug Preparation Technologies Ministry of Education of ChinaCollaborative Innovation Center of New Drug Research and Safety EvaluationZhengzhou UniversityZhengzhou 450052China Key Laboratory of Henan Province for Drug Quality and Evaluation Institute of Drug Discovery and DevelopmentSchool of Pharmaceutical SciencesZhengzhou UniversityZhengzhou 450052China State Key Laboratory of Esophageal Cancer Prevention&Treatment Academy of Medical SciencesZhengzhou UniversityZhengzhou 450052China Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesSt.John’s UniversityQueensNY 11439USA The School of Chinese Medicine The University of Hong KongPokfulamHong KongChina

N6-Methyladenosine(m^(6)A) is the most abundant internal modification in eukaryotic mRNA,playing critical role in various bioprocesses. Like other epigenetic modifications, m^(6)A modification can be catalyzed by the methyltransferase complex and erased dynamically to maintain cells homeostasis. Up to now, only two m^(6)A demethylases have been reported, fat mass and obesity-associated protein(FTO)and alkylation protein AlkB homolog 5(ALKBH5), involving in a wide range of mRNA biological progress, including mRNA shearing, export, metabolism and stability. Furthermore, they participate in many significantly biological signaling pathway, and contribute to the progress and development of cancer along with other diseases. In this review, we focus on the studies about structure, inhibitors development and biological function of FTO and ALKBH5.

关键词： FTO ALKBH5 RNA demethylation Diseases Inhibitors Screening

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Preclinical studies of the triazolo[1,5-a]pyrimidine derivative WS-716 as a highly potent,specific and orally active P-glycoprotein(P-gp)inhibitor

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Acta Pharmaceutica Sinica B 2022年第8期12卷 3263-3280页

作者： Sai-Qi Wang Qiu-Xu Teng Shuai Wang Zi-Ning Lei Hui-Hui Hu Hui-Fang Lv Bei-Bei chen Jian-zheng Wang Xiao-Jing Shi Wei-Feng Xu Hong-Min Liu Xiao-Bing chen zhe-sheng chen Bin Yu Department of Oncology the Affiliated Cancer Hospital of Zhengzhou UniversityHenan Cancer HospitalHenan Cancer InstituteZhengzhou 450008China School of Pharmaceutical Sciences Zhengzhou UniversityZhengzhou 450001China State Key Laboratory of Esophageal Cancer Prevention&Treatment Zhengzhou UniversityZhengzhou 450052China College of Pharmacy and Health Sciences St.John’s UniversityQueensNY 11439USA Laboratory Animal Center Academy of Medical ScienceZhengzhou UniversityZhengzhou 450052China

Multidrug resistance(MDR) is the main cause of clinical treatment failure and poor prognosis in cancer. Targeting P-glycoprotein(P-gp) has been regarded as an effective strategy to overcome MDR. In this work, we reported our preclinical studies of the triazolo[1,5-a]pyrimidine-based compound WS-716 as a highly potent, specific, and orally active P-gp inhibitor. Through direct binding to P-gp,WS-716 inhibited efflux function of P-gp and specifically reversed P-gp-mediated MDR to paclitaxel(PTX) in multiple resistant cell lines, without changing its expression or subcellular localization. WS-716 and PTX synergistically inhibited formation of colony and 3D spheroid, induced apoptosis and cell cycle arrest at G2/M phase in resistant SW620/Ad300 cells. In addition, WS-716 displayed minimal effect on the drug-metabolizing enzyme cytochrome P4503A4(CYP3A4). Importantly, WS-716 increased sensitivity of both pre-clinically and clinically derived MDR tumors to PTX in vivo with the T/C value of 29.7% in patient-derived xenograft(PDX) models. Relative to PTX treatment alone, combination of WS-716 and PTX caused no obvious adverse reactions. Taken together, our preclinical studies revealed therapeutic promise of WS-716 against MDR cancer, the promising data warrant its further development for cancer therapy.

关键词： Multidrug resistance(MDR) ATP-Binding cassette P-gp inhibitors Triazolo[1,5-a]pyrimidine Drug combination Preclinical studies Cancer therapy

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