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2018年中国肿瘤标志物学术大会暨第十二届肿瘤标志物青年科学家论坛

作者： Gang Wang Yibing Chen Qian Wang xiacheng sun Linjie He Lei Zhan Xu Guo Qichao Huang Jinliang Xing 第四军医大学唐都医院普通外科

Objective:It is now widely accepted that mitochondrial biogenesis is inhibited in most cancer cells. Interestingly, one of the possible exceptions is colorectal cancer(CRC), in which the content of mitochondria has been found to be higher than in normal colon mucosa. However, to date,the causes and effects of this phenomenon are still unclear. Methods : In the present study, we systematically investigated the functional role of mitochondrial single-strand DNA binding protein(mtSSB), a key molecule in the regulation of mitochondrial DNA(mtDNA) replication, in the mitochondrial biogenesis and CRC cell growth. First, we determined the expression of mtSSB in paired CRC tissues and investigated the clinical relevance of mtSSB expression. Then the effect of mtSSB on in vitro and in vivo cell proliferation was assessed. We next investigated the effects of mtSSB on mitochondrial biogenesis and functions in CRC cells. Furthermore,we investigated the effects of mtSSB on telomerase activity and telomere elongation. At last, we investigated the function and mechanism of the regulation of proinflammatory cytokines IL-6 on the expression of mtSSB in ***:Our results demonstrated that mtSSB was frequently upregulated in CRC tissues and found that CRC patients with high mtSSB expression had a significantly poorer overall survival and recurrence-free survival than those with low mtSSB expression(Log rank P = 0.025 and 0.006,respectively). We also found that forced expression of mtSSB significantly enhanced the proliferation of CRC cells, while knockdown of mtSSB suppressed the proliferation of CRC cell lines. In addition,xenograft nude mice mode showed that CRC cells with stable mtSSB overexpression exhibited a significant increase in tumorigenesis capacity in vivo, whereas CRC cells with stable mtSSB knockdown exhibited decreased tumorigenesis capacity. Mechanistically, the results showed that overexpression of mtSSB in CRC cells resulted in increased mtDNA content, the coun

关键词： mtSSB mitochondrial biogenesis telomere elongation interleukin 6 reactive oxygen species colorectal cancer

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Decreased MAM formation induced by mitochondrial fission promotes the survival of HCC cells

Decreased MAM formation induced by mitochondrial fission pro...

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2019年中国肿瘤标志物学术大会暨第十三届肿瘤标志物青年科学家论坛

作者： sun,xiacheng Chen,Yanqi Wang,Qian Zhao,Ya Yang,Shirong Bai,Xiangyu Ji,Lele Huang,Qichao Xing,Jinliang State Key Laboratory of Cancer Biology and Experimental Teaching Center of Basic Medicine Fourth Military Medical University Department of General Surgery Tangdu HospitalFourth Military Medical University

Objective Background and Aims:Mitochondria-associated endoplasmic reticulum membrane (MAM) is the junction between the mitochondrial outer membrane and the endoplasmic reticulum membrane,which plays a key role in mediating material transfer and signal transduction between these two *** dynamic balance of mitochondrial division and fusion is closely related to the progress of the HCC and has become one of the hot issues in the field of oncology research in recent years.

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Mitochondrial fission promotes cell migration by Ca2+/CaMKII/ERK/FAK pathway in hepatocellular carcinoma

Mitochondrial fission promotes cell migration by Ca2+/CaMKII...

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2017年中国肿瘤标志物学术大会暨第十一届肿瘤标志物青年科学家论坛

作者： xiacheng sun Haiyan Cao Lei Zhan Gang Wang Jibin Li Zhe Wang Bingrong Liu Qichao Huang Jinliang Xing State Key Laboratory of Cancer Biology and Experimental Teaching Center of Basic Medicine Fourth Military Medical University Department of Gastroenterology Second Affiliated Hospital of Harbin Medical University Department of General Surgery Tangdu HospitalFourth Military Medical University

Background and Aims: Mitochondrial dynamics of fission and fusion plays critical roles in a diverse range of important cellular functions, and its deregulation has been increasingly implicated in human diseases. Previous studies have shown that increased mitochondrial fission significantly promoted the proliferation of hepatocellular carcinoma(HCC) cells. However, how they influence the migration of tumor cells remained largely unknown. Methods: In the present study, we further investigated the effect of mitochondrial fission on the migration and metastasis of HCC cells. Moreover, the underlying molecular mechanisms and therapeutic application were explored. Results: Our data showed that dynamin-1-like protein expression was strongly increased in distant metastasis of HCC when compared to primary HCC. In contrast, the mitochondrial fusion protein mitofusin 1 showed an opposite trend. Moreover, the expression of dynamin-1-like protein and mitofusin 1 was significantly associated with the disease-free survival of HCC patients. In addition, our data further showed that mitochondrial fission significantly promoted the reprogramming of focal adhesion dynamics and lamellipodia formation in HCC cells mainly by activating typical Ca2+/CaMKⅡ/ERK/FAK pathway. Importantly, treatment with mitochondrial division inhibitor-1 significantly decreased calcium signaling in HCC cells and had a potential treatment effect for HCC metastasis in vivo. Conclusions: Taken together, our findings demonstrate that mitochondrial fission plays a critical role in the regulation of HCC cell migration, which provides strong evidence for this process as a drug target in HCC metastasis treatment.

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Upregulation of mtSSB by interleukin-6 promotes cell growth through telomere elongation in colorectal cancer

Upregulation of mtSSB by interleukin-6 promotes cell growth ...

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2017年中国肿瘤标志物学术大会暨第十一届肿瘤标志物青年科学家论坛

作者： Gang Wang Yibing Chen Qian Wang xiacheng sun Haiyan Cao Lei Zhan Xu Guo Jinliang Xing Qichao Huang Xianli He State Key Laboratory of Cancer Biology and Experimental Teaching Center of Basic Medicine Fourth Military Medical University Department of General Surgery Tangdu HospitalFourth Military Medical University Center of Genetic & Prenatal Diagnosis First Affiliated HospitalZhengzhou University Department of Gastroenterology Second Affiliated Hospital of Harbin Medical University

Objectives: Colorectal cancer(CRC) cells rely on mitochondrial oxidative phosphorylation as their source of energy, which depends on sufficient mitochondrial *** single-strand DNA binding protein(mtSSB) plays a critical role in mitochondrial DNA(mtDNA) replication and mitochondrial biogenesis. However, to date, the expression of mtSSB and its potential functional roles in CRC are still unclear. Methods: In the present study, we systematically investigated the functional role of mtSSBin the regulation of CRC cell proliferationin vitro and in *** also explored the underlying molecular mechanisms. Results: Our results demonstrated that mtSSB was frequently upregulated in CRC tissues when compared with non-tumor tissues and upregulated mtSSB was associated with poor prognosis in ***, overexpression ofmtSSB promoted CRC cell survivalin vitroby promoting cell *** vivo assay confirmed these results, indicating that forced expression of mtSSB significantly increased the growth capacity of xenograft tumors, while decreased mtSSB expression was associated with impaired growth capacity of CRC cells in nude ***, the survival advantage conferred by mtSSBwas majorly caused by increasedmitochondrial biogenesis and subsequent ROS production, which induced telomere elongation via activating telomerase in CRC cells. In addition, FOXP1, a member of the forkhead box family, was identified as a new transcription factor for mt SSB. Moreover, our results also demonstrated that proinflammatory IL-6/STAT3 signaling promoted the mtSSB expression and CRC cell proliferation via inducing FOXP1 expression. Conclusion: Collectively, our findings demonstrate that mtSSB plays a critical role in the regulation of CRC proliferation, which provides a strong evidence for this molecule as drug target in CRC treatment.

关键词： mtSSB mitochondrial biogenesis telomere elongation interleukin 6 reactive oxygen species colorectal cancer

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Increased mtDNA copy number promotes cancer progression by enhancing mitochondrial oxidative phosphorylation in microsatellite-stable colorectal cancer

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Signal Transduction and Targeted Therapy 2018年第1期3卷 246-254页

作者： xiacheng sun Lei Zhan Yibing Chen Gang Wang Linjie He Qian Wang Feng Zhou Fang Yang Jin Wu Yousheng Wu Jinliang Xing Xianli He Qichao Huang State Key Laboratory of Cancer Biology and Experimental Teaching Center of Basic Medicine Fourth Military Medical University710032 Xi’anChina Department of Gastroenterology Second Affiliated Hospital of Harbin Medical University150086 HarbinChina Center of Genetic&Prenatal Diagnosis First Affiliated HospitalZhengzhou University450052 ZhengzhouChina Department of General Surgery Tangdu HospitalFourth Military Medical University710032 Xi’anChina Department of General Surgery Huaihai HospitalXuzhou Medical UniversityXuzhou 221004China

Colorectal cancer is one of the leading causes of cancer death *** to global genomic status,colorectal cancer can be classified into two main types:microsatellite-stable and microsatellite-instable ***,the two subtypes also exhibit different responses to chemotherapeutic agents through distinctive molecular ***,mitochondrial DNA depletion has been shown to induce apoptotic resistance in microsatellite-instable colorectal ***,the effects of altered mitochondrial DNA copy number on the progression of microsatellite-stable colorectal cancer,which accounts for the majority of colorectal cancer,remain *** this study,we systematically investigated the functional role of altered mitochondrial DNA copy number in the survival and metastasis of microsatellite-stable colorectal cancer ***,the underlying molecular mechanisms were also *** results demonstrated that increased mitochondrial DNA copy number by forced mitochondrial transcription factor A expression significantly facilitated cell proliferation and inhibited apoptosis of microsatellitestable colorectal cancer cells both in vitro and in ***,we demonstrated that increased mitochondrial DNA copy number enhanced the metastasis of microsatellite-stable colorectal cancer ***,the survival advantage conferred by increased mitochondrial DNA copy number was caused in large part by elevated mitochondrial oxidative ***,treatment with oligomycin significantly suppressed the survival and metastasis of microsatellite-stable colorectal cancer cells with increased mitochondrial DNA copy *** study provides evidence supporting a possible tumor-promoting role for mitochondrial DNA and uncovers the underlying mechanism,which suggests a potential novel therapeutic target for microsatellite-stable colorectal cancer.

关键词： colorectal metastasis inhibited

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Decreased expression of Rab32 promotes hepatocellular carcinoma progression by preventing MAM formation

Decreased expression of Rab32 promotes hepatocellular carcin...

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2022CCTB中国肿瘤标志物学术大会暨中国整合肿瘤学大会暨第十六届肿瘤标志物青年科学家论坛暨中国肿瘤标志物产业创新大会

作者： Xiaoli Liu Zeyu Yan Dalin Wang Jiming Tian Dan Wu Yinping Wang Jing Zhao Qichao Huang Yulu Du Jiniang Xing xiacheng sun Fourth Military Medical University Lanzhou University

Background:Our previous study found that the formation of MAM in HCC cells was reduced and related to the poor patient *** by mass spectrometry revealed that the expression of small GTPase Rab32 in MAM of HCC was significantly *** addition,decreased Rab32 is associated with MAM deficiency and HCC cell viability ***,the mechanism of Rab32 regulates the MAM formation and tumor progression in HCC remains to be systematically ***:We compared Rab32 expression and clinicopathological characteristics using paired HCC and adjacent noncancerous liver tissues from 100 patients by immunohistochemistry ***,cell proliferation,viability and apoptosis were determined in HCC cell lines with Rab32 knockdown or over-expression and MAM formation decrease or increase through EdU,CCK-8 and apoptosis assays,and tumor growth was monitored in nude mice xenograft ***,we systematically investigated the role of Rab32 in regulation of MAM formation by living cell imaging,transmission electron microscope(TEM) and ***:The expression of Rab32 was significantly lower in HCC tissues than in paired peritumor tissues(P<0.01).Specifically,lower expression of Rab32 was found in HCC with more tumor number(P<0.01),larger tumor size(P<0.01),vascular invasion(p<0.05),and advanced TNM stage(P<0.01).Rab32 expression was a prognostic factor for both survival and recurrence after curative *** be specific,functionally,the down-regulation of Rab32 in HCC cells promoted cell proliferation and apoptosis *** contrast,up-regulation of Rab32 obviously inhibited these ***,decreased Rab32 expression could decrease the phosphorylation of the mitochondrial membrane protein,protein tyrosine phosphatase interacting protein-51(PTPIP51) which could interact with the endoplasmic reticulum protein vesicle-associated membrane protein-associated protein B(VAPB) in a PKA-dependent ma

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Increased mtDNA copy number promotes cancer progression by enhancing mitochondrial oxidative phosphorylation in microsatellite stable colorectal cancer

Increased mtDNA copy number promotes cancer progression by e...

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2018年中国肿瘤标志物学术大会暨第十二届肿瘤标志物青...

作者： xiacheng sun Lei Zhan Yibing Chen Gang Wang Linjie He Qian Wang Fang Yang Jin Wu Yousheng Wu Jinliang Xing Xianli He Qichao Huang State Key Laboratory of Cancer Biology and Experimental Teaching Center of Basic Medicine Fourth Military Medical University Department of Gastroenterology Second Affiliated Hospital of Harbin Medical University

Aim:Colorectal cancer（CRC） is one of the leading causes of cancer death in *** to the global genomic status, CRC can be classified into two main types: microsatellite stable（MSS） and microsatellite instable（MSI） tumors. Moreover, the two subtypes also exhibit different responses to chemotherapeutic agents through distinctive molecular mechanisms. Recently,mtDNA depletion has been shown to induce apoptotic resistance in MSI CRC. However, the effects of alternated mtDNA copy number on the progression of MSS CRC, the majority of CRC, remain ***: In this study, we systematically investigated the functional role of altered mtDNA copy number in the survival and metastasis of MSS CRC cells. Moreover, the underlying molecular mechanisms were also explored. Results:Our results demonstrated that increased mtDNA copy number by forced TFAM expression significantly facilitated cell proliferation and inhibited apoptosis of MSS CRC cells both in vitro and in vivo, whereas mtDNA deletion either by TFAM knockdown or ethidium bromide treatment exhibited opposite effects. Moreover, we also demonstrated that increased mtDNA copy number enhanced the metastasis of MSS CRC cells. Mechanistically, the survival advantage conferred by increased mtDNA copy number was majorly caused by the elevated mitochondrial oxidative phosphorylation. Furthermore, treatment with oligomycin（inhibitor of ATP synthase）significantly suppressed the survival and metastasis of MSS CRC cells with increased mtDNA copy number. Conclusion:Our study provides the evidence supporting a possible tumor-promoting role for mtDNA and uncoveres the underlying mechanism, which suggests a potential novel therapeutic target for MSS CRC.

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军事导向型学术交流在军医大学青年教员培养中应用

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实验室研究与探索 2020年第12期39卷 138-141,183页

作者：孙夏承吴菲菲李凯峰田菲张海锋王亚云空军军医大学基础医学实验教学示范中心西安710032

高素质青年教员队伍是实现军医大学培养卫勤保障先锋的重要基础,开展军事导向型学术交流是推进教员队伍建设的一项重要举措。自2019年3月到2020年1月,空军军医大学国家级基础医学实验教学示范中心通过精准聚焦军事医学学术前沿,精心策... 详细信息

高素质青年教员队伍是实现军医大学培养卫勤保障先锋的重要基础,开展军事导向型学术交流是推进教员队伍建设的一项重要举措。自2019年3月到2020年1月,空军军医大学国家级基础医学实验教学示范中心通过精准聚焦军事医学学术前沿,精心策划交叉式学术思想交流,务实打造军事医学特色亮点,共计开展27期学术交流。实践表明,军事导向型学术交流有效促进了军医大学青年师资培养,推动了相关学科与专业建设。

关键词：军医大学军事导向学术交流青年教员教学能力

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线粒体内质网结构偶联介导的线粒体Ca^(2+)摄取及其与肿瘤发生关系研究进展

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中国细胞生物学学报 2018年第12期40卷 2072-2076页

作者：朱子建张嘉煜孙夏承郭欣季乐乐黄启超第四军医大学基础医学院四大队西安710032 第四军医大学基础医学院教学实验中心西安710032 第四军医大学第一附属医院神经内科西安710032

线粒体内质网结构偶联(mitochondria-associated endoplasmic reticulum membranes,MAMs)是线粒体外膜与内质网膜间形成的、具有稳定间距的相互作用膜结构,在介导两细胞器间的物质和信息传递中发挥关键作用。研究表明, MAMs上分布有大量... 详细信息

线粒体内质网结构偶联(mitochondria-associated endoplasmic reticulum membranes,MAMs)是线粒体外膜与内质网膜间形成的、具有稳定间距的相互作用膜结构,在介导两细胞器间的物质和信息传递中发挥关键作用。研究表明, MAMs上分布有大量Ca^(2+)转运通道及相关调控蛋白,可精细调控线粒体Ca^(2+)稳态及ATP生成、细胞凋亡等一系列重要细胞生命活动。进一步研究还发现,MAMs上富集了大量肿瘤相关分子,因此,其参与恶性肿瘤发生的作用机制迅速成为肿瘤基础研究的热点。该文围绕MAMs对线粒体Ca^(2+)摄取及肿瘤发生调控的最新研究进展予以综述,旨在为进一步理解肿瘤发病机制提供新的思路和依据。

关键词：线粒体线粒体内质网结构偶联 Ca^2+信号肿瘤

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基于冗余筛选管控评估机制的移动传感网超宽带稳定传输算法

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电子设计工程 2024年第10期32卷 174-179页

作者：王霞成王恒昆山登云科技职业学院江苏苏州215300 荆楚理工学院电子信息工程学院湖北荆门448000

为了优化WSN网络的数据传输特性,设计了基于冗余筛选管控评估的移动WSN超宽带稳定传输算法。基于冗余传输调度机制对区域予以初次分割,通过能量评估方式快速达到区域聚类稳定生存效果,结合构建区域节点能量阈值的方法提高聚类冗余效率,... 详细信息

为了优化WSN网络的数据传输特性,设计了基于冗余筛选管控评估的移动WSN超宽带稳定传输算法。基于冗余传输调度机制对区域予以初次分割,通过能量评估方式快速达到区域聚类稳定生存效果,结合构建区域节点能量阈值的方法提高聚类冗余效率,以降低超宽带条件下的节点受限概率。采用区域边界控制方式,通过优化骨干节点剩余能量的方式增强骨干节点工作效率,降低因骨干节点而导致的区域传输抖动,确保中继传输节点性能最佳,以降低链路抖动现象。通过骨干节点能力对传输节点予以甄选,从而提升网络链路传输能力,进一步降低抖动现象对传输性能带来的不利影响。仿真实验表明,所提算法具有更低的网络链路累计抖动频次及更好的网络传输带宽。

关键词：移动物联网冗余传输区域边界控制骨干节点

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