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PI3K/AKT/mTOR pathway,hypoxia,and glucose metabolism:Potential targets to overcome radioresistance in small cell lung cancer

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Cancer Pathogenesis and Therapy 2023年第1期1卷 56-66页

作者： Huan Deng Yamei Chen Peijing Li Qingqing Hang Peng Zhang Ying Jin Ming Chen Department of Medical oncology The Cancer Hospital of the University of Chinese Academy of Sciences(Zhejiang Cancer Hospital)HangzhouZhejiang 310022China Department of radiation oncology Zhejiang Key Laboratory of Radiation OncologyHangzhouZhejiang 310022China Department of radiation oncology Institute of Basic Medicine and Cancer(IBMC)Chinese Academy of SciencesHangzhouZhejiang 310022China College of Life Sciences University of the Chinese Academy of SciencesBeijing 100049China Department of radiation oncology Sun Yat-sen University Cancer CenterState Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineSun Yat-sen UniversityGuangzhouGuangdong 510060China

Small cell lung cancer(SCLC)is a highly aggressive tumor type for which limited therapeutic progress has been made.Platinum-based chemotherapy with or without thoracic radiotherapy remains the backbone of treatment,but most patients with SCLC acquire therapeutic resistance.Given the need for more effective therapies,better elucidation of the molecular pathogenesis of SCLC is imperative.The phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway is frequently activated in SCLC and strongly associated with resistance to ionizing radiation in many solid tumors.This pathway is an important regulator of cancer cell glucose metabolism,and its activation probably effects radioresistance by influencing bioenergetic processes in SCLC.Glucose metabolism has three main branches-aerobic glycolysis,oxidative phosphorylation,and the pentose phosphate pathway-involved in radioresistance.The interaction between the PI3K/AKT/mTOR pathway and glucose metabolism is largely mediated by hypoxia-inducible factor 1(HIF-1)signaling.The PI3K/AKT/mTOR pathway also influences glucose metabolism through other mechanisms to participate in radioresistance,including inhibiting the ubiquitination of rate-limiting enzymes of the pentose phosphate pathway.This review summarizes our understanding of links among the PI3K/AKT/mTOR pathway,hypoxia,and glucose metabolism in SCLC radioresistance and highlights promising research directions to promote cancer cell death and improve the clinical outcome of patients with this devastating disease.

关键词： Small cell lung cancer PI3K/AKT/mTOR pathway Glucose metabolism Radioresistance

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High-dose radiation associated with improved survival in IDH-wildtype lowgrade glioma

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Chinese Neurosurgical Journal 2021年第2期7卷 126-130页

作者： Shuai Liu Yanwei Liu Guanzhang Li Jin Feng Li Chen Xiaoguang Qiu Department of radiation oncology Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China Department of molecular Neuropathology Beijing Neurosurgical InstituteCapital Medical UniversityBeijing 100070China

Background:As molecular advances have deepened the knowledge on low-grade glioma(LGG),we investigated the effect of higher radiation dose on the survival of IDH-wildtype(IDHwt)LGG.Methods:In the current study,52 IDHwt LGG patients who received radiotherapy were enrolled from the Chinese Glioma Genome Atlas dataset.radiation doses>54 Gy were defined as high-dose,whereas doses≤54 Gy were defined as low-dose.We performed univariate and multivariate survival analyses to examine the prognostic role of high-dose radiotherapy.Results:In total,the radiation dose ranged from 48.6 Gy to 61.2 Gy,with a median of 55.8 Gy,and 31 patients were grouped into high-dose radiation.Univariate survival analysis indicated that high-dose radiotherapy(p=0.015),tumors located in the frontal lobe(p=0.009),and pathology of astrocytoma(p=0.037)were significantly prognostic factors for overall survival.In multivariate survival analysis,high-dose radiotherapy(p=0.028)and tumors located in the frontal lobe(p=0.016)were independently associated with better overall survival.Conclusions:In conclusion,high-dose radiotherapy independently improved the survival of IDHwt LGG.This can guide treatments for glioma with known molecular characteristics.

关键词： radiation dose IDH-wildtype Low-grade glioma Survival

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CDK11 negatively regulates Wnt/β-catenin signaling in the endosomal compartment by affecting microtubule stability

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Cancer Biology & Medicine 2020年第2期17卷 328-342页

作者： Danmin Ou Lin Chen Jiang He Zhuoxian Rong Jie Gao Liyu Liu Feiyu Tang Jiang Li Yuezhen Deng Lunquan Sun Department of oncology Center for Molecular MedicineXiangya HospitalCentral South UniversityChangsha 410008China international Cooperation Base of Cancer Precision Therapy Department of Science and Technology of Hunan ProvinceChangsha 410008China Key Laboratory of molecular radiation oncology of Hunan Province Changsha 410008China National Clinical Research Center for Geriatric Disorders Changsha 410008China

Objectives:Improper activation of Wnt/β-catenin signaling has been implicated in human diseases.Beyond the well-studied glycogen synthase kinase 3p(GSK3p)and casein kinase 1(CK1),other kinases affecting Wnt/β-catenin signaling remain to be defined.Methods:To identify the kinases that modulate Wnt/β-catenin signaling,we applied a kinase small interfering RNA(siRNA)library screen approach.Luciferase assays,immunoblotting,and real-time polymerase chain reaction(PCR)were performed to confirm the regulation o f the Wnt/β-catenin signaling pathway by cyclin-dependent kinase 11(CDK11)and to investigate the underlying mechanism.Confocal immunofluorescence,coimmunoprecipitation(co-IP),and scratch wound assays were used to demonstrate colocalization,detect protein interactions,and explore the function of CDK11.Results:CDK11 was found to be a significant candidate kinase participating in the negative control of Wnt/P-catenin signaling.Down-regulation of CDK11 led to the accumulation of Wnt/β-catenin signaling receptor complexes,in a manner dependent on intact adenomatosis polyposis coli(APC)protein.Further analysis showed that CDK11 modulation of Wnt/P-catenin signaling engaged the endolysosomal machinery,and CDK11 knockdown enhanced the colocalization of Wnt/β-catenin signaling receptor complexes with early endosomes and decreased colocalization with lysosomes.Mechanistically,CDK11 was found to function in Wnt/β-catenin signaling by regulating microtubule stability.Depletion of CDK11 down-regulated acetyl-a-tubulin.Moreover,co-IP assays demonstrated that CDK11 interacts with the a-tubulin deacetylase SIRT2,whereas SIRT2 down-regulation in CDK11-depleted cells reversed the accumulation of Wnt/(3-catenin signaling receptor complexes.CDK11 was found to suppress cell migration through altered W nt/β-catenin signaling.Conclusions:CDK11 is a negative modulator of Wnt/β-catenin signaling that stabilizes microtubules,thus resulting in the dysregulation of receptor complex trafficking from early endosomes to lysosomes.

关键词： Wnt/β-catenin signaling CDK11 endosome microtubule SIRT2

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DNA Damage, Signaling and Repair: Protecting genomic integrity and reducing the risk of human disease

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Chinese Science Bulletin 2011年第30期56卷 3119-3121页

作者： ZHOU PingKun Department of radiation Toxicology and oncology, Beijing Institute of radiation Medicine, Beijing 100850, China Special Topic Editor Department of radiation Toxicology and oncology Beijing Institute of Radiation Medicine

DNA is the genetic material that contains the 'instructions' to not only guide the continuation of life but also govern the development, metabolism and functioning of living organisms. DNA damage occurs daily due to v... 详细信息

关键词： DNA损伤基因组伤信号人类疾病整性修复风险保护

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放射敏感的纳米调节剂重新编程肿瘤-免疫细胞通讯用于免疫治疗

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Science China Materials 2023年第1期66卷 352-362页

作者：陈园园刘淑杰高鹏潘伟石明婉王建波李娜唐波 College of Chemistry Chemical Engineering and Materials ScienceKey Laboratory of Molecular and Nano ProbesMinistry of EducationCollaborative Innovation Center of Functionalized Probes for Chemical Imaging in Universities of ShandongInstitute of Molecular and Nano ScienceShandong Normal UniversityJinan 250014China Department of radiation oncology Qilu HospitalCheeloo College of MedicineShandong UniversityJinan 250012China

目前,将肿瘤相关巨噬细胞从促肿瘤生长的M2表型调节为抑制肿瘤生长的M1表型已成为一种有前途的肿瘤免疫治疗策略,但仍然具有挑战性,而且以可控的方式实现显得尤为困难.在此,我们报道了一种用于可时空激活免疫反应的放射敏感型纳米调节剂... 详细信息

目前,将肿瘤相关巨噬细胞从促肿瘤生长的M2表型调节为抑制肿瘤生长的M1表型已成为一种有前途的肿瘤免疫治疗策略,但仍然具有挑战性,而且以可控的方式实现显得尤为困难.在此,我们报道了一种用于可时空激活免疫反应的放射敏感型纳米调节剂(AuDAP).AuDAP可通过多价相互作用同时识别和结合M2巨噬细胞与肿瘤细胞.在低剂量医用X射线照射下,纳米调节剂可介导产生大量活性氧(ROS),激活NF-κB信号通路,使M2型巨噬细胞复极化为M1型,从而原位激活巨噬细胞的免疫功能.一系列体外和体内实验结果表明,纳米调节剂可以有效重塑肿瘤细胞和巨噬细胞之间的通讯,并特异性地激活抗肿瘤免疫治疗.通过长时间观察发现,治疗组小鼠的原位肿瘤被明显抑制且未观察到肺部转移瘤的形成.该纳米调节剂可作为一种有潜力的纳米药物用于精确的肿瘤治疗,并能为可控的免疫治疗提供新的见解.

关键词：肿瘤免疫治疗 M2型巨噬细胞肿瘤相关巨噬细胞复极化免疫细胞肿瘤治疗纳米药物体内实验

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Oligometastases in prostate cancer:Ablative treatment

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World Journal of Clinical oncology 2019年第2期10卷 38-51页

作者： Amalia Palacios-Eito Amelia Béjar-Luque Milagrosa Rodríguez-Li?án Sonia García-Cabezas Department of radiation oncology Reina Sofia University Hospital

Technological advances in radiotherapy have led to the introduction of techniques such as stereotactic body radiation therapy(SBRT), allowing the administration of ablative doses. The hypothesis that oligometastatic disease may be cured through local eradication therapies has led to the increasing use of SBRT in patients with this type of disease. At the same time, scientific advances are being made to allow the confirmation of clinically suspected oligometastatic status at molecular level. There is growing interest in identifying patients with oligometastatic prostate cancer(PCa) who may benefit from curative intent metastasis-directed therapy, including SBRT. The aim is to complement, replace or delay the introduction of hormone therapy or other systemic therapies. The present review aims to compile the evidence from the main ongoing studies and results on SBRT in relation to oligometastatic PCa; examine aspects where gaps in knowledge or a lack of consensus persist(e.g., optimum schemes, response assessment, identification and diagnosis of oligometastatic patients); and document the lack of first-level evidence supporting the use of such techniques.

关键词： Oligometastases Metastasis-directed therapy Stereotactic body radiation therapy Stereotactic ablative radiotherapy Prostate cancer

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Inhibition of tumor suppressor p73 by nerve growth factor receptor via chaperone-mediated autophagy

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Journal of molecular Cell Biology 2020年第9期12卷 700-712页

作者： Daniel Nguyen Kun Yang Lucia Chiao Yun Deng Xiang Zhou Zhen Zhang Shelya X.Zeng Hua Lu Department of Biochemistry and molecular Biology Tulane Cancer CenterTulane University School of MedicineNew OrleansLA 70112USA Department of radiation oncology Shanghai Cancer CenterDepartment of OncologyShanghai Medical SchoolFudan UniversityShanghai 200032China Present address:Verna and Marrs McLean Department of Biochemistry and molecular Biology Baylor College of MedicineHoustonTX 77030USA Present address:Department of radiation oncology Shanghai Cancer CenterFudan UniversityShanghai 200032China Present address:Institute of Biomedical Sciences Shanghai Cancer CenterFudan UniversityShanghai 200032China

The tumor suppressr p73 is a homolog of p53 and is capable of inducing cell cycle arrest and apoptosis.Here,we identify nerve growth factor receptor(NGFR,p75NTR,or CD271)as a novel negative p73 regulator.p73 activates NGFR transcription,which,in turn,promotes p73 degradation in a negative feedback loop.NGFR directly binds to p73 central DNA-binding domain and suppresses p73 transcriptional activity as well as p73-mediated apoptosis in cancer cells.Surprisingly,we uncover a previously unknown mechanism of NGFR-facilitated p73 degradation through the chaperone-mediated autophagy(CMA)pathway.Collectively,our studies demonstrate a new oncogenic function for NGFR in inactivating p73 activity by promoting its degradation through the CMA.

关键词： p73 NGFR chaperone-mediated autophagy Lamp2a HSPA8

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Long noncoding RNAs in prostate cancer： overview and clinical implications

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Asian Journal of Andrology 2016年第4期18卷 568-574页

作者： Bhavna Malik Felix Y Feng Department of radiation oncology University of Michigan Ann Arbor Michigan USA Department of radiation oncology Urology and Medicine University of California at San Francisco USA Helen Diller Family Comprehensive Cancer Center University of California at San Francisco USA

Prostate cancer is the second most common cause of cancer mortality among men in the United States. While many prostate cancers are indolent, an important subset of patients experiences disease recurrence after conventional therapy and progresses to castration-resistant prostate cancer （CRPC）, which is currently incurable. Thus, there is a critical need to identify biomarkers that will distinguish indolent from aggressive disease, as well as novel therapeutic targets for the prevention or treatment of CRPC. In recent years, long noncoding RNAs （IncRNAs） have emerged as an important class of biological molecules. LncRNAs are polyadenylated RNA species that share many similarities with protein-coding genes despite the fact that they are noncoding （not translated into proteins）. They are usually transcribed by RNA polymerase II and exhibit the same epigenetic signatures as protein-coding genes. LncRNAs have also been implicated in the development and progression of variety of cancers, including prostate cancer. While a large number of IncRNAs exhibit tissue- and cancer-specific expression, their utility as diagnostic and prognostic biomarkers is just starting to be explored. In this review, we highlight recent findings on the functional role and molecular mechanisms of IncRNAs in the progression of prostate cancer and evaluate their use as potential biomarkers and therapeutic targets.

关键词： biomarker long noncoding RNAs （IncRNAs） prostate cancer

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Nuclear medical molecular imaging of tumor angiogenesis： current status and future prospects

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Chinese Medical Journal 2013年第14期126卷 2741-2746页

作者： HU Xu-dong XING Li-gang YU Jin-ming Department of radiation oncology Key Laboratory of Radiation Oncology of Shandong Province Shandong Tumor Hospital & Institute Jinan Shandong 250117 China Postdoctoral Working Station of Tianjin Medical University Tianjin 300072 China

Objective To review the current status and progress on nuclear medical molecular imaging of angiogenesis. Data sources A literature search was performed in Medline and PubMed published in English up to May 31, 2012. The search terms were molecular imaging, nuclear medicine and angiogenesis. Study selection Articles studying molecular imaging of angiogenesis using radionuclide were selected and reviewed. Results molecular imaging has been used for studying angiogenesis by targeting integrin aVI33, VEGF/VEGFR, and matrix metalloproteinases （MMPs） with radionuclide-labeled tracers. The technology has been shown to be able to assess the angiogenesis status and/or predict the efficacy of anti-angiogenic therapy. Future directions of the research on the molecular imaging of angiogenesis include development of new tracers with better tumor targeting efficacy, desirable pharmacokinetics, and easy translation to clinical applications. Conclusion Advances in molecular imaging of angiogenesis using radioculcide will make the technology a valuable tool for personalized anti-angiogenesis treatment.

关键词： molecular imaging nuclear medicine angiogenesis

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Advances in molecular,genetic and immune signatures of gastric cancer:Are we ready to apply them in our patients' decision making?

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World Journal of Gastrointestinal oncology 2018年第7期10卷 172-183页

作者： Stavros Gkolfinopoulos Demetris Papamichael Konstantinos Papadimitriou Panos Papanastasopoulos Vassilios Vassiliou Panteleimon Kountourakis Demetris Papamichael Panos PapanastasopoulosPanteleimon KountourakisDepartment of Medical OncologyBOC Oncology CenterNicosia 2006Cyprus Department of Medical oncology University Hospital of AntwerpAntwerp 2650Belgium Department of radiation oncology BOC Oncology CenterNicosia 2006Cyprus

In the last few years we have witnessed a vast expansion of our knowledge regarding the molecular and genetic profile of gastric cancer.The molecular subtypes described have shed light on the pathogenesis of the disease,thus prompting the development of new therapeutic strategies and favoring a more individualized approach for treatment.Most of the clinical trials for so called targeted therapies could be considered,at best,partially successful.In addition,checkpoint inhibitors ha-ve recently been added to our armamentarium in later stages of the disease,and combinations with chemotherapy and targeted agents are currently under development.In view of the rapid advances of molecular oncology,a new challenge for the clinical oncologist arises: The appropriate patient selection for each new therapy,which can be made possible only through the implementation of predictive biomarkers in our therapy decision making.

关键词： Gastric cancer Cancer Genome Atlas Asian Cancer Research Group Targeted therapy

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