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A small-molecule pan-HER inhibitor alone or in combination with Cisplatin exerts efficacy against nasopharyngeal carcinoma

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Frontiers of Medicine 2023年第2期17卷 275-289页

作者： Jing Yang Yanfei Yang Yuquan Wei Xiawei Wei Laboratory of Aging Research and Cancer Drug Target State Key Laboratory of Biotherapy and Cancer CenterNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengdu 610041China Melanoma and Sarcoma Medical Oncology Unit State Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China State Key Laboratory of Oncology in South China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China Department of Gynecology and Obstetrics The Third Xiangya HospitalCentral South UniversityChangsha 410008China

The abnormal activation of HER family kinase activity is closely related to the development of human malignancies.In this study,we used HER kinases as targets for the treatment of nasopharyngeal carcinoma(NPC)and explored the anti-tumor effects of the novel pan-HER inhibitor HM781-36B,alone or in combination with Cisplatin.We found that HER family proteins were positively expressed in tumor tissues of some NPC patients,and the high levels of those proteins were significantly related to poor prognosis.HM781-36B inhibited NPC in vitro and in vivo.HM781-36B exerted synergistic effects with Cisplatin on inhibiting proliferation and promoting apoptosis of NPC cells.In NPC xenograft models in nude mice,HM781-36B and Cisplatin synergistically inhibited tumor growth.Downregulating the activity of HER family proteins and their downstream signaling pathways and regulating tumor microenvironment may explain the synergistic anti-tumor effects of HM781-36B and Cisplatin.In conclusion,our study provides evidence for HER family proteins as prognostic biomarkers and potential therapeutic targets for NPC.The pan-HER inhibitor HM781-36B alone or in combination with Cisplatin represents promising therapeutic effects for the treatment of NPC patients,which provides a new idea for the comprehensive treatment of NPC.

关键词： epidermal growth factor receptor ErbB receptors HM781-36B nasopharyngeal carcinoma molecular targeted therapy Cisplatin

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Niclosamide(NA)overcomes Cisplatin resistance in human ovarian cancer

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Genes & Diseases 2023年第4期10卷 1687-1701页

作者： Linjuan Huang Jing Zhang Youling Deng Hao Wang Piao Zhao Guozhi Zhao Wei Zeng Yonghui Wang Connie Chen William Wagstaff Rex C.Haydon Russell R.Reid Tong-Chuan He Le Shen Hue H.Luu Ling Zhao Departments of Obstetrics and Gynecology Orthopaedic Surgery and UrologyThe First Affiliated Hospital of Chongqing Medical UniversityChongqing 400046China Molecular Oncology Laboratory Department of Orthopaedic Surgery and Rehabilitation MedicineThe University of Chicago Medical CenterChicagoIL 60637USA Ministry of Education Key Laboratory of Diagnostic Medicine and Department of Clinical BiochemistryThe School of Laboratory MedicineChongqing Medical UniversityChongqing 400016China Department of Neurology The Second Affiliated Hospital of Jianghan UniversityWuhanHubei 430050China Department of Clinical Laboratory Medicine Shanghai Jiaotong University School of MedicineShanghai 200000China Laboratory of Craniofacial Suture Biology and Development Department of Surgery Section of Plastic SurgeryThe University of Chicago Medical CenterChicagoIL 60637USA Department of Surgery The University of Chicago Medical CenterChicagoIL 60637USA

Ovarian cancer(OC)is one of the most lethal malignancies of the female reproduc-tive system.OC patients are usually diagnosed at advanced stages due to the lack of early diag-nosis.The standard treatment for OC includes a combination of debulking surgery and platinum-taxane chemotherapy,while several targeted therapies have recently been approved for maintenance treatment.The vast majority of OC patients relapse with chemoresistant tu-mors after an initial response.Thus,there is an unmet clinical need to develop new therapeu-tic agents to overcome the chemoresistance of OC.The anti-parasite agent niclosamide(NA)has been repurposed as an anti-cancer agent and exerts potent anti-cancer activities in human cancers including OC.Here,we investigated whether NA could be repurposed as a therapeutic agent to overcome Cisplatin-resistant(CR)in human OC cells.To this end,we first established two CR lines SKOV3CR and OVCAR8CR that exhibit the essential biological characteristics of Cisplatin resistance in human cancer.We showed that NA inhibited cell proliferation,sup-pressed cell migration,and induced cell apoptosis in both CR lines at a low micromole range.Mechanistically,NA inhibited multiple cancer-related pathways including AP1,ELK/SRF,HIF1,and TCF/LEF,in SKOV3CR and OVCAR8CR cells.NA was further shown to effectively inhibit xenograft tumor growth of SKOV3CR cells.Collectively,our findings strongly suggest that NA may be repurposed as an efficacious agent to combat Cisplatin resistance in chemoresistant hu-man OC,and further clinical trials are highly warranted.

关键词： Chemotherapy resistance Cisplatin Drug repurposing Niclosamide Ovarian cancer

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Inhibition of histone methyltransferase PRMT5 attenuates Cisplatininduced hearing loss through the PI3K/Akt-mediated mitochondrial apoptotic pathway

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Journal of Pharmaceutical Analysis 2023年第6期13卷 590-602页

作者： Zhiwei Zheng Benyu Nan Chang Liu Dongmei Tang Wen Li Liping Zhao Guohui Nie Yingzi He ENT Institute and Department of Otorhinolaryngology Eye&ENT HospitalState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceNHC Key Laboratory of Hearing Medicine(Fudan University)Fudan UniversityShanghai200031China Department of Otorhinolaryngology-Head and Neck Surgery The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical UniversityWenzhou325000ZhejiangChina Department of Otolaryngology-Head and Neck Surgery The Third Affiliated Hospital of Sun Yat-Sen UniversityGuangzhou510630China Department of Otolaryngology Shenzhen Institute of Translational MedicineShenzhen Second People's HospitalThe First Affiliated Hospital of Shenzhen UniversityShenzhen518035GuangdongChina

This study aimed to evaluate the therapeutic potential of inhibiting protein arginine methyltransferase 5(PRMT5)in Cisplatin-induced hearing loss.The effects of PRMT5 inhibition on Cisplatin-induced auditory injury were determined using immunohistochemistry,apoptosis assays,and auditory brainstem response.The mechanism of PRMT5 inhibition on hair cell survival was assessed using RNA-seq and Cleavage Under Targets and Tagment-quantitative polymerase chain reaction(CUT&Tag-qPCR)analyses in the HEI-OC1 cell line.Pharmacological inhibition of PRMT5 significantly alleviated Cisplatin-induced damage to hair cells and spiral ganglion neurons in the cochlea and decreased apoptosis by protecting mitochondrial function and preventing the accumulation of reactive oxygen species.CUT&Tag-qPCR analysis demonstrated that inhibition of PRMT5 in HEI-OC1 cells reduced the accumulation of H4R3me2s/H3R8me2s marks at the promoter region of the Pik3ca gene,thus activating the expression of Pik3ca.These findings suggest that PRMT5 inhibitors have strong potential as agents against Cisplatininduced ototoxicity and can lay the foundation for further research on treatment strategies of hearing loss.

关键词： Protein arginine methyltransferase 5 (PRMT5) LLY-283 Cisplatin Hearing loss Hair cell Spiral ganglion neuron

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Astaxanthine attenuates Cisplatin ototoxicity in vitro and protects against Cisplatin-induced hearing loss in vivo

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Acta Pharmaceutica Sinica B 2022年第1期12卷 167-181页

作者： Benyu Nan Zirui Zhao Kanglun Jiang Xi Gu Huawei Li Xinsheng Huang Department of Otorhinolaryngology-Head and Neck Surgery Zhongshan HospitalFudan UniversityShanghai 200030China Department of Otorhinolaryngology-Head and Neck Surgery Wenzhou Medical UniversityAffiliated Hospital 2Wenzhou 325000China Department of Otolaryngology Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghai 200437China Department of Otolaryngology the First Affiliated Hospital of Fujian Medical UniversityFuzhou 350005China ENT Institute and Department of Otorhinolaryngology Eye&ENT HospitalState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceFudan UniversityShanghai 200031China Institutes of Biomedical Sciences Fudan UniversityShanghai 200031China NHC Key Laboratory of Hearing Medicine(Fudan University) Shanghai 200031China The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science Fudan UniversityShanghai 200031China

Astaxanthine(AST) has important biological activities including antioxidant and antiinflammatory effects that could alleviate neurological and heart diseases, but its role in the prevention of Cisplatin-induced hearing loss(CIHL) is not yet well understood. In our study, a steady interaction between AST and the E3 ligase adapter Kelch-like ECH-associated protein 1, a predominant repressor of nuclear factor erythroid 2-related factor 2(NRF2), was performed and tested via computer molecular docking and dynamics. AST protected against Cisplatin-induced ototoxicity via NRF2 mediated pathwayusing quantitative PCR and Western blotting. The levels of reactive oxygen species(ROS) and mitochondrial membrane potential revealed that AST reduced ROS overexpression and mitochondrial dysfunction.Moreover, AST exerted anti-apoptosis effects in mouse cochlear explants using immunofluorescence staining and HEI-OC1 cell lines using quantitative PCR and Western blotting. Finally, AST combined with poloxamer was injected into the middle ear through the tympanum, and the protection against CIHL was evaluated using the acoustic brain stem test and immunofluorescent staining in adult mice. Our results suggest that AST reduced ROS overexpression, mitochondrial dysfunction, and apoptosis via NRF2-mediated pathway in Cisplatin-exposed HEI-OC1 cell lines and mouse cochlear explants, finally promoting cell survival. Our study demonstrates that AST is a candidate therapeutic agent for CIHL.

关键词： Astaxanthine Cisplatin Hearing loss Mitochondrial Ototoxicity Reactive oxygen species Apoptosis

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“Pincer movement”:Reversing Cisplatin resistance based on simultaneous glutathione depletion and glutathione S-transferases inhibition by redox-responsive degradable organosilica hybrid nanoparticles

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Acta Pharmaceutica Sinica B 2022年第4期12卷 2074-2088页

作者： Boyi Niu Yixian Zhou Kaixin Liao Ting Wen Sixian Lao Guilan Quan Xin Pan Chuanbin Wu School of Pharmaceutical Sciences Sun Yat-sen UniversityGuangzhou 510006China College of Pharmacy Jinan UniversityGuangzhou 510632China

The therapeutic efficacy of Cisplatin has been restricted by drug resistance of cancers.Intracellular glutathione(GSH)detoxification of Cisplatin under the catalysis of glutathione S-transferases(GST)plays important roles in the development of Cisplatin resistance.Herein,a strategy of“pincer movement”based on simultaneous GSH depletion and GST inhibition is proposed to enhance Cisplatin-based chemotherapy.Specifically,a redox-responsive nanomedicine based on disulfide-bridged degradable organosilica hybrid nanoparticles is developed and loaded with Cisplatin and ethacrynic acid(EA),a GST inhibitor.Responding to high level of intracellular GSH,the hybrid nanoparticles can be gradually degraded due to the break of disulfide bonds,which further promotes drug release.Meanwhile,the disulfide-mediated GSH depletion and EA-induced GST inhibition cooperatively prevent cellular detoxification of Cisplatin and reverse drug resistance.Moreover,the nanomedicine is integrated into microneedles for intralesional drug delivery against Cisplatin-resistant melanoma.The in vivo results show that the nanomedicine-loaded microneedles can achieve significant GSH depletion,GST inhibition,and consequent tumor growth suppression.Overall,this research provides a promising strategy for the construction of new-type nanomedicines to overcome Cisplatin resistance,which extends the biomedical application of organosilica hybrid nanomaterials and enables more efficient chemotherapy against drug-resistant cancers.

关键词： Cancer therapy Cisplatin Drug resistance Glutathione depletion Glutathione Stransferases Disulfide bonds Organosilica hybrid nanoparticles Ethacrynic acid

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CD209 signaling pathway as a biomarker for Cisplatin chemotherapy response in small cell lung cancer

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Genes & Diseases 2024年第3期11卷 11-14页

作者： Anqi Lin Hong Yang Jian Zhang Peng Luo Department of Oncology Zhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong 510282China The First Clinical Medical School Southern Medical UniversityGuangzhouGuangdong 510515China

One of the bottlenecks in the clinical treatment of small cell lung cancer(SCLC)is its susceptibility to multidrug resistance.While SCLC is sensitive to platinum-based chemotherapy at the initial stage of treatment,it can rapidly become drug-resistant,allowing tumor growth to accelerate.A significant decrease in drug sensitivity after recurrence and multidrug resistance can seriously interfere with the effectiveness of treatment,making sensitivity maintenance one of the urgent challenges to be solved.Therefore,discovering prognostic markers for Cisplatin chemotherapy and understanding the mechanisms of Cisplatin resistance have great practical significance for improving the outcomes of sCLC patients.

关键词： Cisplatin chemotherapy lung

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Inhibiting DNA methylation alleviates Cisplatininduced hearing loss by decreasing oxidative stress-induced mitochondria-dependent apoptosis via the LRP1-PI3K/AKT pathway

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1305-1321页

作者： Yingzi He Zhiwei Zheng Chang Liu Wen Li Liping Zhao Guohui Nie Huawei Li ENT Institute and Otorhinolaryngology Department of Eye&ENT Hospital State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceFudan UniversityShanghai 200031China NHC Key Laboratory of Hearing Medicine(Fudan University) Shanghai 200031China Department of Otolaryngology and Institute of Translational Medicine Shenzhen Second People’s Hospital/the First Affiliated Hospital of Shenzhen University Health Science CenterShanghai 200032China Institutes of Biomedical Sciences Fudan UniversityShanghai 200032China The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science Fudan UniversityShenzhen 518035China

Cisplatin-related ototoxicity is a critical side effect of chemotherapy and can lead to irreversible hearing loss.This study aimed to assess the potential effect of the DNA methyltransferase(DNMT)inhibitor RG108 on Cisplatin-induced ototoxicity.Immunohistochemistry,apoptosis assay,and auditory brainstem response(ABR)were employed to determine the impacts of RG108 on Cisplatin-induced injury in murine hair cells(HCs)and spiral ganglion neurons(SGNs).Rhodamine 123 and TMRM were utilized for mitochondrial membrane potential(MMP)assessment.Reactive oxygen species(ROS)amounts were evaluated by Cellrox green and Mitosox-red probes.Mitochondrial respiratory function evaluation was performed by determining oxygen consumption rates(OCRs).The results showed that RG108 can markedly reduce Cisplatin induced damage in HCs and SGNs,and alleviate apoptotic rate by protecting mitochondrial function through preventing ROS accumulation.Furthermore,RG108 upregulated BCL-2 and downregulated APAF1,BAX,and BAD in HEI-OC1 cells,and triggered the PI3K/AKT pathway.Decreased expression of low-density lipoprotein receptor-related protein 1(LRP1)and high methylation of the LRP1 promoter were observed after Cisplatin treatment.RG108 treatment can increase LRP1expression and decrease LRP1 promoter methylation.In conclusion,RG108 might represent a new potential agent for preventing hearing loss induced by Cisplatin via activating the LRP1-PI3K/AKT pathway.

关键词： Cisplatin DNMT Apoptosis Hair cell Spiral ganglion neurons RG108 Mitochondrial dysfunction ROS

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Synergistic effects of silver nanoparticles and Cisplatin in combating inflammation and hyperplasia of airway stents

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Bioactive Materials 2022年第3期7卷 266-280页

作者： Zhaonan Li Chuan Tian Dechao Jiao Jing Li Yahua Li Xueliang Zhou Huiping Zhao Yanan Zhao Xinwei Han Department of Interventional Radiology First Affiliated Hospital of Zhengzhou UniversityZhengzhou450001PR China Department of Radiology First Affiliated Hospital of Zhengzhou UniversityZhengzhou450001PR China

Anti-inflammatory and antihyperplasia activities are essential requirements for the successful use of airway stents.In this work,silver nanoparticles(AgNPs)and Cisplatin(DDP)were combined in a synergistic modification strategy to improve the surface function of airway stents.Using polycaprolactone(PCL)as a drug carrier,a dual-functional PCL-AgNPs-DDP fiber film-coated airway stent was fabricated by electrospinning.The physicochemical and biological properties of the obtained fiber films were examined.The ATR-FTIR,XPS,SEM-EDS and TEM results suggested that AgNPs and DDP could be successfully immobilized onto the airway stent surface.The drug release and surface degradation results revealed that AgNPs and DDP can undergo sustained release from films for 30 d,and the weight loss was approximately 50%after 35 d.In addition,the dual-functional fiber film suppressed human embryonic lung fibroblast growth and exhibited excellent antibacterial activity against Staphylococcus aureus,Pseudomonas aeruginosa and Candida albicans.Furthermore,the effectiveness of the dual-functional fiber film-coated airway stent was evaluated by application to the trachea of New Zealand rabbits.The in vivo results indicated that PCL-AgNPs-DDP fiber film-coated airway stent can significantly inhibit granulation tissue formation and collagen deposition,reduced the expression of IL-8,TNF-α,IL-1α,PCNA,α-SMA and CD68,and ultimately achieved anti-inflammatory and antihyperplasia effects.Hence,this study provides a dual-functional surface-coated airway stent to address the clinical complications associated with respiratory tract inflammation and granulation tissue hyperplasia,thus inhibiting tracheal stenosis.

关键词： Anti-inflammatory Antihyperplasia Airway stent Silver nanoparticle Cisplatin

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TOPK Activation Exerts Protective Effects on Cisplatin-induced Acute Kidney Injury

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Current Medical Science 2022年第4期42卷 742-753页

作者： Hui ZHANG Qing-qing DONG Hua-pan SHU Yu-chi TU Qian-qian LIAO Li-jun YAO Department of Nephrology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

Objective:T-LAK-cell-originated protein kinase(TOPK),a PSD95-Disc large-ZO1(PDZ)binding kinase(PBK),is a novel member of the mitogen-activated protein kinase(MAPK)family.Studies have shown that TOPK plays a critical role in the function of tumor cells,including apoptosis and mitosis.However,little is known on the effect of TOPK in Cisplatin-induced acute kidney injury(CP-AKI).This study aimed to investigate the role and mechanism of TOPK in CPAKI.Methods:Cisplatin was administered to C57BL/6 mice and cultured kidney tubular epithelial cells(TECs)to establish the CP-AKI murine or cellular models.TECs were then stimulated with the specific inhibitor of TOPK OTS514 or transfected with the recombinant-activated plasmid TOPK-T9E to inhibit or activate TOPK.The TECs were treated with AKT inhibitorⅧfollowing stimulation with OTS514 or Cisplatin.Western blotting and flow cytometry were used to evaluate the cell cycle and apoptosis of TECs.Results:The analysis revealed that the TOPK activity was significantly suppressed by Cisplatin,both in vivo and in vitro.Furthermore,the pharmacological inhibition of TOPK by OTS514,a specific inhibitor of TOPK,exacerbated the Cisplatin-induced cell cycle arrest in the G2/M phase and apoptosis of cultured TECs.Moreover,the TOPK activation via the TOPK-T9E plasmid transfection could partially reverse the cell cycle arrest at the G2/M phase and apoptosis of Cisplatin-treated TECs.In addition,AKT/protein kinase B(PKB),as a TOPK target protein,was inhibited by Cisplatin in cultured TECs.The pharmaceutical inhibition of AKT further aggravated the apoptosis of TECs induced by Cisplatin or TOPK inhibition.TOPK systematically mediated the apoptosis via the AKT pathway in the CP-AKI cell model.Conclusion:These results indicate that TOPK activation protects against CP-AKI by ameliorating the G2/M cell cycle arrest and cell apoptosis.

关键词： acute kidney injury Cisplatin cell cycle apoptosis T-LAK-cell-originated protein kinase/PSD95-Disc large-ZO1 binding kinase

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Ellagic acid ameliorates Cisplatin-induced acute kidney injury by regulating inflammation and SIRT6/TNF-α signaling

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Food Science and Human Wellness 2023年第6期12卷 2232-2241页

作者： Yuqi Gao Kezheng Peng Yida Wang Yannan Guo Chenye Zeng Rui Hua Qingfei Liu Xue Li Ying Qiu Zhao Wang The Ministry of Education Key Laboratory of Protein Science School of Pharmaceutical SciencesTsinghua UniversityBeijing 100084China School of Medicine Tsinghua UniversityBeijing 100084China

De spite Cisplatin has been widely used in the treatment of various cancers,the noteworthy nephrotoxicity greatly constrained its clinical value.For this reason,finding novel targeted therapies to attenuate the nephrotoxicity of Cisplatin should be pretty significant.Our previous study found that histone deacetylase sirtuin 6(SIRT6)could be an ideal target for the treatment of Cisplatin-induced acute kidney injury.In this study,we explored the protective effects of ellagic acid,a natural polyphenol compound that activates SIRT6,on Cisplatin-induced nephrotoxicity.Pre-treatment of ellagic acid attenuated cytotoxicity of Cisplatin in primary renal cells and TCMK-1 cells.Moreover,ellagic acid ameliorated renal dysfunction,apoptosis and fibrosis induced by Cisplatin in mice.Furthermore,ellagic acid reduced nephrotoxicity-associated inflammatory factor interleukin(IL)-1βand IL-6 expression both in vitro and in vivo.Mechanistically,ellagic acid reversed Cisplatin-reduced SIRT6 expression and diminished Cisplatin-induced tumor necrosis factor(TNF)-αexpression.And SIRT6 knockdown abrogated the protective effects of ellagic acid on Cisplatin-induced cell apoptosis,indicating the renal-protective effects of ellagic acid are mainly dependent on ellagic acid-mediated SIRT6 activation.Our results provide preclinical rationale for using ellagic acid as a feasible and promising agent to ameliorate Cisplatin-induced acute kidney injury,and support ellagic acid as a potential adjunctive therapy for future cancer treatment.

关键词： Ellagic acid Nephrotoxicity Cisplatin SIRT6 TNF-α

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