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Tanshinone IIA Suppresses Non-Small Cell Lung Cancer Through beclin-1-Mediated Autophagic Apoptosis

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Engineering 2022年第12期19卷 128-138页

作者： Shasha Bai Sainan Cui Wenhao Wen Elaine Lai-Han Leung Jing Bai Huiyuan Lin Yongfei Cui Lei Yang Zhongqiu Liu Yuan Zheng Rong Zhang School of Pharmaceutical Sciences Guangzhou University of Chinese MedicineGuangzhou 510006China State Key Laboratory of Quality Research in Chinese Medicine/Macao Institute for Applied Research in Medicine and Health Macao University of Science and TechnologyMacao 999078China Cardiothoracic Surgery Department The Second Clinical College of Guangzhou University of Chinese MedicineGuangdong Provincial Hospital of Chinese MedicineGuangzhou 510006China

It is necessary to develop a new strategy for treatment of lung cancer since it is the main cause of cancer *** IIA(Tan IIA),an active ingredient of a commonly used traditional Chinese herb Salvia miltiorrhiza,provides a new direction to develop a new strategy for the *** has been found that Tan IIA could inhibit lung cancer in vitro and in vivo by inducing autophagic *** IIA increased apoptotic cells and the expression of cleaved caspase 3 and cleaved caspase 9,decreased B-cell lymphoma-2(Bcl-2)/Bcl-2 associated X protein(Bax)ratio in human non-small cell lung cancer(NSCLC)cell lines,which was promoted by an autophagy activator Rapamycin,and weaken by autophagy inhibitor 3-methyladenine(3-MA).In addition,Tan IIA induced more autophagosomes,up-regulated light chain 3b(LC-3B)I and LC-3B II conversion and less sequestosome 1(SQSTM1/p62)expression,which cannot be weakened by the caspase 3 ***,overexpression of LC-3B gene(LC3B)and downregulation of autophagic gene 5(ATG5)further confirmed that Tan IIA induced autophagic apoptosis in NSCLC cell ***-1 gene(BECN1)overexpression and silence attenuated the effects of Tan IIA,suggesting autophagic apoptosis that Tan IIA induced was dependent on ***,our study demonstrated a new treatment mechanism of Tan IIA and suggested that Tan IIA is a potential new anti-cancer therapeutic option.

关键词： Tan IIA Autophagy Apoptosis beclin-1

Piceatannol enhances beclin-1 activity to suppress tumor progression and its combination therapy strategy with everolimus in gastric cancer

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Science China(Life Sciences) 2023年第2期66卷 298-312页

作者： Longtao Huangfu Xiaoyang Wang Shanshan Tian Junbing Chen Xueying Wang Biao Fan Qian Yao Gangjian Wang Cong Chen Jing Han Xiaofang Xing Jiafu Ji Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education) Division of Gastrointestinal Cancer Translational Research LaboratoryPeking University Cancer Hospital&InstituteBeijing 100142China Department of Pharmacy Peking University Cancer Hospital&InstituteBeijing 100142China National Institute on Drug Dependence Peking UniversityBeijing 100191China Gastrointestinal Cancer Center Peking University Cancer Hospital&InstituteBeijing 100142China Department of Pathology Peking University Cancer Hospital&InstituteBeijing 100142China

The effects and regulation of beclin-1-an autophagy-related protein-have not been fully defined, however, a negative correlation has been reported between beclin-1 expression and carcinogenesis. Meanwhile, no compound has been shown to directly inhibit its activity. Here, we evaluate piceatannol, a naturally occurring polyphenolic compound, as a potential targeting agonist of beclin-1, to assess its efficacy as an antitumor agent against gastric cancer. More specifically, we determine the effects of piceatannol treatment on cell viability using a monitoring system and colony forming assay. Piceatannol was found to efficiently inhibit the proliferation of several human gastric cancer cell lines. Autophagic flux is increased by piceatannol treatment, and correlates with inhibition of cell proliferation and colony formation. Additionally, microscale thermophoresis and surface plasmon resonance results show a direct interaction between piceatannol and beclin-1, which reduces the phosphorylation activity of beclin-1 at the Ser-295 site. Notably, piceatannol impairs the binding of beclin-1 to Bcl-2 and enhances the recruitment of binding of UV radiation resistance-associated gene protein, which further triggers beclin-1-dependent autophagy signaling. An increase in autophagic activity via treatment with the mTOR inhibitor, everolimus, effectively sensitizes piceatannol-induced antitumor effects. Xenograft models confirmed that piceatannol inhibits tumor development and elicits a potent synergistic effect with everolimus in vivo. Taken together, the findings of this study strongly support the application of combinatorial piceatannol and everolimus therapy in future clinical trials for gastric cancer patients.

关键词： piceatannol beclin-1 autophagy everolimus gastric cancer drug synergy

Predictive and prognostic implications of 4E-BP1, beclin-1, and LC3for cetuximab treatment combined with chemotherapy in advanced colorectal cancer with wild-type KRAS: Analysis from real-world data

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World Journal of Gastroenterology 2019年第15期25卷 1840-1852页

作者： Gui-Fang Guo Yi-Xing Wang Yi-Jun Zhang Xiu-Xing Chen Jia-Bin Lu Hao-Hua Wang Chang Jiang Hui-Quan Qiu Liang-Ping Xia VIP Department Sun Yat-sen University Cancer Center Collaborative Innovation Center for Cancer Medicine State Key Laboratory of Oncology in South China Sun Yat-sen University Cancer Center Pathology Department Sun Yat-sen University Cancer Center

BACKGROUND Colorectal cancer(CRC) is one of the main causes of cancer-related deaths in China and around the world. Advanced CRC(ACRC) patients suffer from a low cure rate though treated with targeted therapies. The response rate is about 50% to chemotherapy and cetuximab, a monoclonal antibody targeting epidermal growth factor receptor(EGFR) and used for ACRC with wild-type KRAS. It is important to identify more predictors of cetuximab efficacy to further improve precise treatment. Autophagy, showing a key role in the cancer progression, is influenced by the EGFR pathway. Whether autophagy can predict cetuximab efficacy in ACRC is an interesting *** To investigate the effect of autophagy on the efficacy of cetuximab in colon cancer cells and ACRC patients with wild-type *** ACRC patients treated with cetuximab plus chemotherapy, with detailed data and tumor tissue, at Sun Yat-sen University Cancer Center from January 1, 2005,to October 1, 2015, were studied. Expression of autophagy-related proteins[beclin1, microtubule-associated protein 1 A/B-light chain 3(LC3), and 4 Ebinding protein 1(4 E-BP1)] was examined by Western blot in CRC cells and by immunohistochemistry in cancerous and normal tissues. The effect of autophagy on cetuximab-treated cancer cells was confirmed by MTT assay. The associations between beclin1, LC3, and 4 E-BP1 expression in tumor tissue and the efficacy of cetuximab-based therapy were *** In CACO-2 cells exposed to cetuximab, LC3 and 4 E-BP1 were upregulated, and P62 was downregulated. Autophagosome formation was observed, and autophagy increased the efficacy of cetuximab. In 68 ACRC patients,immunohistochemistry showed that beclin1 levels were significantly correlated with those of LC3(0.657, P 1) and 4 E-BP1(0.211, P = 0.042) in ACRC ***3 was significantly overexpressed in tumor tissues compared to normal tissues(P 1). In 45 patients with wild-type KRAS, the expression levels of these three pro

关键词： 4E-binding protein 1 beclin-1 Microtubule-associated protein 1A/B-light chain 3 Advanced colorectal cancer Cetuximab efficacy Prognosis

beclin-1基因沉默对蛇六谷提取物损伤胃癌SGC-7901细胞的影响

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中国病理生理杂志 2019年第3期35卷 436-441页

作者：潘磊胡梦奕李赛陈培丰尹利明浙江中医药大学附属第一医院浙江杭州310006 宁波市中医院浙江宁波315010

目的:探讨beclin-1基因沉默对蛇六谷提取物损伤人胃癌SGC-7901细胞的影响。方法:采用携带beclin-1-shRNA的慢病毒载体感染胃癌SGC-7901细胞,敲减beclin-1基因表达;蛇六谷提取物处理beclin-1基因敲减和未敲减的SGC-7901细胞,CCK-8法检测... 详细信息

目的:探讨beclin-1基因沉默对蛇六谷提取物损伤人胃癌SGC-7901细胞的影响。方法:采用携带beclin-1-shRNA的慢病毒载体感染胃癌SGC-7901细胞,敲减beclin-1基因表达;蛇六谷提取物处理beclin-1基因敲减和未敲减的SGC-7901细胞,CCK-8法检测细胞活力,流式细胞术分析细胞凋亡率,Western blot检测beclin-1和LC3的蛋白表达水平。结果:beclin-1-shRNA转染SGC-7901细胞抑制beclin-1的mRNA和蛋白表达,促进LC3蛋白表达,降低细胞活力,增加细胞凋亡率(P1细胞的beclin-1和LC3蛋白表达,但下调beclin-1基因敲减的SGC-7901细胞的LC3蛋白表达,并显著降低细胞活力和增加细胞凋亡率(Pbeclin-1基因沉默阻断蛇六谷提取物对beclin-1相关信号通路的激活,增强蛇六谷提取物对胃癌SGC-7901细胞活力的损伤作用。

关键词：蛇六谷胃癌 beclin-1 基因沉默细胞活力

beclin-1 shRNA对低氧诱导的SH-SY5Y细胞自噬的影响

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中国应用生理学杂志 2018年第5期34卷 464-469页

作者：卢娜李成长罗晓秋杨坤丽新乡医学院生理学与神经生物学教研室河南新乡453003

目的:构建beclin-1基因短发夹干扰RNA(shRNA)慢病毒载体,感染人SH-SY5Y细胞,观察沉默beclin-1基因后低氧对SH-SY5Y细胞自噬的影响。方法:构建特异性靶向beclin-1基因的shRNA慢病毒表达载体和阴性对照序列慢病毒载体;再将载体转染入SH-S... 详细信息

目的:构建beclin-1基因短发夹干扰RNA(shRNA)慢病毒载体,感染人SH-SY5Y细胞,观察沉默beclin-1基因后低氧对SH-SY5Y细胞自噬的影响。方法:构建特异性靶向beclin-1基因的shRNA慢病毒表达载体和阴性对照序列慢病毒载体;再将载体转染入SH-SY5Y细胞; RT-PCR检测beclin-1的mRNA表达; Western blot检测beclin-1蛋白表达; CCK-8法测定beclin-1 shRNA对SH-SY5Y细胞活力的影响。再将空白对照、阴性对照、转染型三种细胞分别以21%常氧及5%低氧培养,Western blot检测各组细胞LC3蛋白表达;电镜观察自噬小体。结果:beclin-1 shRNA能明显抑制SH-SY5Y细胞beclin-1的mRNA及蛋白的表达;沉默beclin-1基因后,beclin-1 shRNA组细胞存活率与阴性对照组相比无差异;成功建立了稳定表达beclin-1 shRNA的SH-SY5Y细胞。5%低氧处理后,与阴性对照组相比较,beclin-1 shRNA组细胞中LC3Ⅱ/LC3Ⅰ比值下调,细胞内自噬小体数量减少。结论:慢病毒介导的beclin-1shRNA对SH-SY5Y细胞的活力无影响,但可以抑制低氧诱导的自噬。

关键词： SH-SY5Y beclin-1 自噬短发夹RNA

Bcl-2和beclin-1在胰腺癌中的表达及其相关性研究

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四川大学学报（医学版） 2012年第2期43卷 156-160页

作者：曹双双苏安平杜晓炯李昂胡伟明张肇达田伯乐陆慧敏柯能文何兆鹏四川大学华西医院肝胆胰外科成都610041

目的探讨Bcl-2和beclin-1在胰腺癌发生发展过程中的作用,分析胰腺癌组织中Bcl-2和beclin-1的蛋白表达是否具有相关性。方法收集胰腺癌、胰腺外分泌良性肿瘤、慢性胰腺炎、正常胰腺组织各6例,分别标记为A组、B组、C组、D组。采用实时荧... 详细信息

目的探讨Bcl-2和beclin-1在胰腺癌发生发展过程中的作用,分析胰腺癌组织中Bcl-2和beclin-1的蛋白表达是否具有相关性。方法收集胰腺癌、胰腺外分泌良性肿瘤、慢性胰腺炎、正常胰腺组织各6例,分别标记为A组、B组、C组、D组。采用实时荧光定量PCR检测各组中Bcl-2mRNA和beclin-1mRNA表达情况。采用免疫组织化学法检测各组中Bcl-2蛋白及beclin-1蛋白的表达情况。结果 A、B、C 3组Bcl-2mRNA和蛋白表达水平均高于D组,其中A组表达水平最高,与其它各组比较差异有统计学意义(Pbeclin-1mRNA和蛋白表达水平低于D组,差异有统计学意义(P0.05);其中A组表达水平最低,D组表达水平最高。胰腺癌中Bcl-2和beclin-1蛋白的表达呈负相关(r=-0.827,P=0.042)。结论胰腺癌组织中Bcl-2表达水平上调,抑制凋亡,beclin-1表达水平下调,抑制自噬。Bcl-2和beclin-1在胰腺癌中表达呈负相关,两者共同作用可促进胰腺癌的发生发展。

关键词： Bcl-2 beclin-1 胰腺癌凋亡自噬

beclin-1非自噬依赖性通路在肿瘤中的研究进展

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生命科学 2019年第8期31卷 795-801页

作者：应杰王梦张蒙梁朝朝安徽医科大学第一附属医院泌尿外科合肥230022 深圳大学附属罗湖医院泌尿外科深圳518000

beclin-1作为重要的自噬调节因子在肿瘤发生和进展过程中起到重要作用。然而近年来越多越多的研究揭示,除调控自噬外,beclin-1还可通过非自噬依赖性通路调控生长因子受体信号通路、协助细胞有丝分裂、促进DNA损伤修复以及间接促进肿瘤... 详细信息

beclin-1作为重要的自噬调节因子在肿瘤发生和进展过程中起到重要作用。然而近年来越多越多的研究揭示,除调控自噬外,beclin-1还可通过非自噬依赖性通路调控生长因子受体信号通路、协助细胞有丝分裂、促进DNA损伤修复以及间接促进肿瘤细胞凋亡进程,进而影响肿瘤发生和进展。该文将对beclin-1在肿瘤中的非自噬依赖性功能进行综述。

关键词： beclin-1 肿瘤非自噬依赖性通路

Omi/beclin-1通路在离心运动致骨骼肌自噬中的作用

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中国组织工程研究 2018年第36期22卷 5791-5796页

作者：雷槟恺孙君志赵晓琴丁海丽刘永王瑞元李俊平成都体育学院运动医学与健康学院四川省成都市610041 北京体育大学运动人体科学学院北京市100084 太原理工大学体育学院山西省太原市030024

背景:离心运动会导致骨骼肌自噬水平改变,使骨骼肌超微结构发生改变,影响骨骼肌正常的收缩活动。目的:观察离心运动后不同时程骨骼肌细胞自噬的情况及Omi/beclin-1信号通路的变化,以探究运动对骨骼肌自噬的影响及可能机制。方法:将32只... 详细信息

背景:离心运动会导致骨骼肌自噬水平改变,使骨骼肌超微结构发生改变,影响骨骼肌正常的收缩活动。目的:观察离心运动后不同时程骨骼肌细胞自噬的情况及Omi/beclin-1信号通路的变化,以探究运动对骨骼肌自噬的影响及可能机制。方法:将32只健康雄性大鼠分为安静对照组(8只),离心运动组(24只)。离心运动组完成一次性跑台运动(坡度为-16°,速度为16 m/min,时间为90 min),在运动后即刻、24 h、48 h取材(各8只),使用Western blot方法检测各组不同时程Lc3-Ⅱ、Omi、HAX-1、beclin-1蛋白表达水平。结果与结论:(1)离心运动后,Lc3-Ⅱ、Omi、beclin-1蛋白表达显著升高;Lc3-Ⅱ和Omi蛋白表达在运动后即刻达到最高峰;beclin-1在运动后24 h到达峰值;(2)离心运动后,HAX-1蛋白表达显著降低,在24 h达到最低,之后开始恢复;运动后48 h与安静组相比差异无显著性意义;(3)结果显示:离心运动可以导致骨骼肌细胞自噬增强,可能通过上调Omi/beclin-1信号通路所致。

关键词：离心运动骨骼肌自噬 Omi beclin-1 组织构建

温和灸对神经根型颈椎病大鼠脊髓beclin-1/Bcl-2表达的影响

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针刺研究 2020年第10期45卷 799-805页

作者：蔡慧倩粟胜勇张熙覃美相黄小珍代琪蒋香玉林安黄梅广西中医药大学第一临床医学院南宁530001 广西中医药大学第一附属医院针灸科南宁530023

目的:观察温和灸对神经根型颈椎病(CSR)大鼠脊髓(包括神经根组织)自噬和凋亡因子beclin-1、Bcl-2mRNA及蛋白表达的影响,探讨温和灸“大椎”对CSR大鼠的镇痛机制。方法:将SD大鼠随机分为空白组、模型组、温和灸组、温和灸+3-methyladenin... 详细信息

目的:观察温和灸对神经根型颈椎病(CSR)大鼠脊髓(包括神经根组织)自噬和凋亡因子beclin-1、Bcl-2mRNA及蛋白表达的影响,探讨温和灸“大椎”对CSR大鼠的镇痛机制。方法:将SD大鼠随机分为空白组、模型组、温和灸组、温和灸+3-methyladenine(3-MA)组,每组10只。除空白组外,其他3组大鼠均采用插线入颈神经根的方法制备CSR模型。空白组大鼠仅正常饲养,不做任何干预;模型组只注射0.9%氯化钠溶液干预;温和灸组予温和灸“大椎”,10min/次,并腹腔注射0.9%氯化钠溶液;温和灸+3-MA组予温和灸“大椎”并注射3-MA干预。3组均从造模后第3天开始连续干预7d,1次/d。观察各组大鼠步态评分;用疼痛分析仪测量各组大鼠的痛阈值;用荧光定量PCR法检测各组大鼠脊髓(包括神经根)组织中beclin-1、Bcl-2mRNA的表达;用免疫组织化学法检测脊髓(包括神经根)组织中beclin-1、Bcl-2蛋白的表达水平;用透射电镜观察脊髓神经根组织自噬小体及超微结构。结果:与空白组比较,造模后模型组大鼠步态评分升高(P1),机械痛阈值降低(P1)。干预后,与模型组比较,温和灸组及温和灸+3-MA组大鼠的步态评分明显降低(P1),痛阈值及大鼠脊髓组织beclin-1、Bcl-2mRNA与蛋白表达均明显升高(P1,Pbeclin-1、Bcl-2表达,激活细胞的自噬、抑制细胞凋亡有关。

关键词：神经根型颈椎病温和灸自噬 beclin-1 Bcl-2