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Breast cancer
Potentiation of the Anticancer Effects by Combining Docetaxel with Ku-0063794 against Triple-Negative Breast Cancer Cells
Ye-Won Jeon, Ok-Hee Kim, Jin Sun Shin, Ha Eun Hong, Cho Hee Kim, Say-June Kim
Cancer Res Treat. 2022;54(1):157-173.   Published online April 5, 2021
DOI: https://doi.org/10.4143/crt.2020.1063
AbstractAbstract PDFPubReaderePub
Purpose
mTORC1 and mTORC2 inhibition by Ku-0063794 could confer profound anticancer effects against cancer cells because it eliminates feedback activation of Akt. Herein, we aimed to determine anticancer effects of docetaxel and Ku-0063794, individually or in combination, against breast cancer cells, especially triple-negative breast cancer (TNBC) cells.
Materials and Methods
MCF-7 breast cancer and MDA-MB-231 TNBC cell lines for in vitro studies and mouse xenograft model for in vivo studies were used to investigate the effect of docetaxel, Ku-0063794, or their combination.
Results
In the in vitro experiments, combination therapy synergistically reduced cell viability and induced higher apoptotic cell death in breast cancer cells than the individual monotherapies (p < 0.05). Western blot analysis and flow cytometric analysis showed that the combination therapy induced higher apoptotic cell death than the individual monotherapies (p < 0.05). In the in vivo experiment, docetaxel and Ku-0063794 combination therapy reduced the growth of MDA-MB-231 cells xenografted in the nude mice better than in the individual monotherapies (p < 0.05). Immunohistochemistry showed that the combination therapy induced the highest expression of cleaved caspase-3 and the lowest expression of Bcl-xL in the MDA-MB-231 cells xenografted in the nude mice (p < 0.05). Western blot analysis and immunofluorescence, incorporating both in vitro and in vivo experiments, consistently validated that unlike individual monotherapies, docetaxel and Ku-0063794 combination therapy significantly inhibited epithelial-mesenchymal transition (EMT) and autophagy (p < 0.05).
Conclusion
These data suggest that docetaxel and Ku-0063794 combination therapy has higher anticancer activities over individual monotherapies against MDA-MB-231 TNBC cells through a greater inhibition of autophagy and EMT.

Citations

Citations to this article as recorded by  
  • Phosphatidic acid as a cofactor of mTORC1 in platinum-based chemoresistance: Mechanisms and therapeutic potential
    Hadi Alizadeh, Sana Kerachian, Keyvan Jabbari, Bahram Mohammad Soltani
    European Journal of Pharmacology.2025; 988: 177220.     CrossRef
  • Comprehensive analysis of the function of helicobacter-associated ferroptosis gene YWHAE in gastric cancer through multi-omics integration, molecular docking, and machine learning
    Dingwei Liu, Jianxiang Peng, Jun Xie, Yong Xie
    Apoptosis.2024; 29(3-4): 439.     CrossRef
  • Targeting autophagy drug discovery: Targets, indications and development trends
    Mengjia Jiang, Wayne Wu, Zijie Xiong, Xiaoping Yu, Zihong Ye, Zhiping Wu
    European Journal of Medicinal Chemistry.2024; 267: 116117.     CrossRef
  • Characterization of BCL-XL, MCL-1, and BAX Protein Expression in Response to Neoadjuvant Chemotherapy in Breast Cancer
    Tareq Saleh, Sofian Al Shboul, Heyam Awad, Mohammed El-Sadoni, Ahmad Alhesa, Elham Alsharaiah, Nisreen Abu Shahin, Moureq R. Alotaibi, AbdelKader Battah, Bilal Azab
    Applied Immunohistochemistry & Molecular Morphology.2024; 32(4): 189.     CrossRef
  • Autophagy modulation in cancer therapy: Challenges coexist with opportunities
    Yongya Wu, Aoxue Wang, Guotai Feng, Xiaoli Pan, Wen Shuai, Panpan Yang, Jing Zhang, Liang Ouyang, Yi Luo, Guan Wang
    European Journal of Medicinal Chemistry.2024; 276: 116688.     CrossRef
  • Research progress and development strategy of PI3K inhibitors for breast cancer treatment: A review (2016-present)
    Rujue Peng, Yujie Zhan, Anqi Li, Qiaoli Lv, Shan Xu
    Bioorganic Chemistry.2024; 153: 107934.     CrossRef
  • EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions
    Mehrdad Hashemi, Hamid Zaferani Arani, Sima Orouei, Shayan Fallah, Amin Ghorbani, Maryam Khaledabadi, Amirabbas Kakavand, Alireza Tavakolpournegari, Hamidreza Saebfar, Hajar Heidari, Shokooh Salimimoghadam, Maliheh Entezari, Afshin Taheriazam, Kiavash Hus
    Biomedicine & Pharmacotherapy.2022; 155: 113774.     CrossRef
  • 6,985 View
  • 263 Download
  • 8 Web of Science
  • 7 Crossref
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Head/neck cancer
Protective Effects of N-Acetylcysteine against Radiation-Induced Oral Mucositis In Vitro and In Vivo
Haeng Jun Kim, Sung Un Kang, Yun Sang Lee, Jeon Yeob Jang, Hami Kang, Chul-Ho Kim
Cancer Res Treat. 2020;52(4):1019-1030.   Published online June 18, 2020
DOI: https://doi.org/10.4143/crt.2020.012
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Radiation-induced oral mucositis limits delivery of high-dose radiation to targeted cancers. Therefore, it is necessary to develop a treatment strategy to alleviate radiation-induced oral mucositis during radiation therapy. We previously reported that inhibiting reactive oxygen species (ROS) generation suppresses autophagy. Irradiation induces autophagy, suggesting that antioxidant treatment may be used to inhibit radiation-induced oral mucositis.
Materials and Methods
We determined whether treatment with N-acetyl cysteine (NAC) could attenuate radiation-induced buccal mucosa damage in vitro and in vivo. The protective effects of NAC against oral mucositis were confirmed by transmission electron microscopy and immunocytochemistry. mRNA and protein levels of DNA damage and autophagy-related genes were measured by quantitative real-time polymerase chain reaction and western blot analysis, respectively.
Results
Rats manifesting radiation-induced oral mucositis showed decreased oral intake, loss of body weight, and low survival rate. NAC intake slightly increased oral intake, body weight, and the survival rate without statistical significance. However, histopathologic characteristics were markedly restored in NAC-treated irradiated rats. LC3B staining of rat buccal mucosa revealed that NAC treatment significantly decreased the number of radiation-induced autophagic cells. Further, NAC inhibited radiation-induced ROS generation and autophagy signaling. In vitro, NAC treatment significantly reduced the expression of NRF2, LC3B, p62, and Beclin-1 in keratinocytes compared with that after radiation treatment.
Conclusion
NAC treatment significantly inhibited radiation-induced autophagy in keratinocytes and rat buccal mucosa and may be a potentially safe and effective option for the prevention of radiation-induced buccal mucosa damage.

Citations

Citations to this article as recorded by  
  • N-Acetyl-L-Cysteine Protects Organ Function After Hemorrhagic Shock Combined With Seawater Immersion in Rats by Correcting Coagulopathy and Acidosis
    Yiyan Liu, Yu Zhu, Zisen Zhang, Daiqin Bao, Haoyue Deng, Liangming Liu, Tao Li
    Frontiers in Physiology.2022;[Epub]     CrossRef
  • Nutraceuticals as Modulators of Autophagy: Relevance in Parkinson’s Disease
    Michał Rakowski, Szymon Porębski, Agnieszka Grzelak
    International Journal of Molecular Sciences.2022; 23(7): 3625.     CrossRef
  • Oxidative Stress and Chemoradiation-Induced Oral Mucositis: A Scoping Review of In Vitro, In Vivo and Clinical Studies
    Huynh Nguyen, Simran Sangha, Michelle Pan, Dong Ha Shin, Hayoung Park, Ali I. Mohammed, Nicola Cirillo
    International Journal of Molecular Sciences.2022; 23(9): 4863.     CrossRef
  • A Minireview on Gastrointestinal Microbiota and Radiosusceptibility
    Aihong Mao, Chao Sun, Takanori Katsube, Bing Wang
    Dose-Response.2020;[Epub]     CrossRef
  • 9,496 View
  • 261 Download
  • 11 Web of Science
  • 4 Crossref
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An Integrated Nomogram Combining Clinical Factors and Microtubule-Associated Protein 1 Light Chain 3B Expression to Predict Postoperative Prognosis in Patients with Intrahepatic Cholangiocarcinoma
Liang Chen, Hongyuan Fu, Tongyu Lu, Jianye Cai, Wei Liu, Jia Yao, Jinliang Liang, Hui Zhao, Jiebin Zhang, Jun Zheng, Yingcai Zhang, Yang Yang
Cancer Res Treat. 2020;52(2):469-480.   Published online October 7, 2019
DOI: https://doi.org/10.4143/crt.2019.423
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Microtubule-associated protein 1 light chain 3B (LC3B) serves as a key component of autophagy, which is associated with the progression of carcinoma. Yet, it is still unclear whether LC3B is also an independent risk factor for intrahepatic cholangiocarcinoma (ICC). We aim to explore the predictive value of LC3B on prognosis of ICC, and to establish a novel and available nomogram to predict relapse-free survival (RFS) and overall survival (OS) for these patients after curative-intent hepatectomy.
Materials and Methods
From August 2004 to March 2017, 105 ICC patients were eligibly enrolled in the Third Affiliated Hospital of Sun Yat-sen University. Preoperative clinical information of enrolled patients was collected. Expression LC3B in the ICC specimen was detected by immunohistochemistry.
Results
The 5-year RFS and OS in this cohort were 15.7% and 29.6%, respectively. On multivariate Cox regression analysis, independent risk factors for 5-year OS were cancer antigen 125, microvascular invasion, LC3B expression and lymph node metastasis. Except for the above 4 factors, neutrophil/lymphocyte ratio and tumor differentiation were independent factors for 5-year RFS. The area under the curve of nomograms for OS and RFS were 0.820 and 0.747, respectively.
Conclusion
The nomograms based on LC3B can be considered as effective models to predict postoperative survival for ICC patients.

Citations

Citations to this article as recorded by  
  • Lymph node metastasis of intrahepatic cholangiocarcinoma: the present and prospect of detection and dissection
    Ruoyu Zhang, Yunfei Tan, Mei Liu, Liming Wang
    European Journal of Gastroenterology & Hepatology.2024; 36(12): 1359.     CrossRef
  • Active Autophagy Is Associated with Favorable Outcome in Patients with Surgically Resected Cholangiocarcinoma
    Katrin Bankov, Falko Schulze, Steffen Gretser, Henning Reis, Nada Abedin, Fabian Finkelmeier, Jörg Trojan, Stefan Zeuzem, Andreas A. Schnitzbauer, Dirk Walter, Peter J. Wild, Maximilian N. Kinzler
    Cancers.2023; 15(17): 4322.     CrossRef
  • The role and implication of autophagy in cholangiocarcinoma
    Hayat Khizar, Yufei Hu, Yanhua Wu, Jianfeng Yang
    Cell Death Discovery.2023;[Epub]     CrossRef
  • Immunogenomics of cholangiocarcinoma
    Virag Gehl, Colm J. O’Rourke, Jesper B. Andersen
    Hepatology.2023;[Epub]     CrossRef
  • Multiparametric MRI‐Based Radiomic Signature for Preoperative Evaluation of Overall Survival in Intrahepatic Cholangiocarcinoma After Partial Hepatectomy
    Yang Yang, Xianlun Zou, Wei Zhou, Guanjie Yuan, Daoyu Hu, Dong Kuang, Yaqi Shen, Qingguo Xie, Qingpeng Zhang, Xuemei Hu, Zhen Li
    Journal of Magnetic Resonance Imaging.2022; 56(3): 739.     CrossRef
  • A Myeloid Signature-Based Nomogram Predicts the Postoperative Recurrence of Intrahepatic Cholangiocarcinoma
    Jing Liang, Hui Zhou, Xiang-Qi Huang, Yan-Fei Liu, Lei Zhang, Dan He, Yongmei Cui, Jinrui Guo, Kunpeng Hu, Chong Wu
    Frontiers in Molecular Biosciences.2021;[Epub]     CrossRef
  • Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma
    Hector Perez-Montoyo
    Cells.2020; 9(3): 614.     CrossRef
  • 7,916 View
  • 185 Download
  • 8 Web of Science
  • 7 Crossref
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Pan-Pim Kinase Inhibitor AZD1208 Suppresses Tumor Growth and Synergistically Interacts with Akt Inhibition in Gastric Cancer Cells
Miso Lee, Kyung-Hun Lee, Ahrum Min, Jeongeun Kim, Seongyeong Kim, Hyemin Jang, Jee Min Lim, So Hyeon Kim, Dong-Hyeon Ha, Won Jae Jeong, Koung Jin Suh, Yae-Won Yang, Tae Yong Kim, Do-Youn Oh, Yung-Jue Bang, Seock-Ah Im
Cancer Res Treat. 2019;51(2):451-463.   Published online June 6, 2018
DOI: https://doi.org/10.4143/crt.2017.341
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Pim kinases are highly conserved serine/threonine kinases, and different expression patterns of each isoform (Pim-1, Pim-2, and Pim-3) have been observed in various types of human cancers, including gastric cancer. AZD1208 is a potent and selective inhibitor that affects all three isoforms of Pim. We investigated the effects of AZD1208 as a single agent and in combination with an Akt inhibitor in gastric cancer cells.
Materials and Methods
The antitumor activity of AZD1208 with/without an Akt inhibitor was evaluated in a large panel of gastric cancer cell lines through growth inhibition assays. The underlying mechanism was also examined by western blotting, immunofluorescence assay, and cell cycle analysis.
Results
AZD1208 treatment decreased gastric cancer cell proliferation rates and induced autophagy only in long-term culture systems. Light chain 3B (LC3B), a marker of autophagy, was increased in sensitive cells in a dose-dependent manner with AZD1208 treatment, which suggested that the growth inhibition effect of AZD1208 was achieved through autophagy, not apoptosis. Moreover, we found that cells damaged by Pim inhibition were repaired by activation of the DNA damage repair pathway, which promoted cell survival and led the cells to become resistant to AZD1208. We also confirmed that the combination of an Akt inhibitor with AZD1208 produced a highly synergistic effect in gastric cancer cell lines.
Conclusion
Treatment with AZD1208 alone induced considerable cell death through autophagy in gastric cancer cells. Moreover, the combination of AZD1208 with an Akt inhibitor showed synergistic antitumor effects through regulation of the DNA damage repair pathway.

Citations

Citations to this article as recorded by  
  • A literature review of recent advances in gastric cancer treatment: exploring the cross-talk between targeted therapies
    Reza Panahizadeh, Padideh Panahi, Vahid Asghariazar, Shima Makaremi, Ghasem Noorkhajavi, Elham Safarzadeh
    Cancer Cell International.2025;[Epub]     CrossRef
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    Yuzhen Li, Lang Shi, Fan Zhao, Yanwen Luo, Mingjiao Zhang, Xiongfei Wu, Jiefu Zhu
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    Hongtao Duan, Li Gao, Aiminuer Asikaer, Lingzhi Liu, Kuilong Huang, Yan Shen
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    Ping Lin, Lingyan He, Nan Tian, Xuchen Qi
    Journal of Cancer Research and Clinical Oncology.2023; 149(13): 12413.     CrossRef
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    Feng‐Ze Yan, Ying‐Chun Ouyang, Tie‐Gang Meng, Hong‐Yong Zhang, Wei Yue, Xin‐Ran Zhang, Yue Xue, Zhen‐Bo Wang, Qing‐Yuan Sun
    Journal of Cellular Physiology.2022; 237(9): 3661.     CrossRef
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    Aanchal Rathi, Dhiraj Kumar, Gulam Mustafa Hasan, Mohammad Mahfuzul Haque, Md Imtaiyaz Hassan
    Biochimica et Biophysica Acta (BBA) - General Subjects.2021; 1865(11): 129995.     CrossRef
  • TDP1 and TOP1 Modulation in Olaparib-Resistant Cancer Determines the Efficacy of Subsequent Chemotherapy
    Jin Won Kim, Ahrum Min, Seock-Ah Im, Hyemin Jang, Yu Jin Kim, Hee-Jun Kim, Kyung-Hun Lee, Tae-Yong Kim, Keun Wook Lee, Do-Youn Oh, Jee-Hyun Kim, Yung-Jue Bang
    Cancers.2020; 12(2): 334.     CrossRef
  • PIM1 (Moloney Murine Leukemia Provirus Integration Site) Inhibition Decreases the Nonhomologous End-Joining DNA Damage Repair Signaling Pathway in Pulmonary Hypertension
    Marie-Claude Lampron, Géraldine Vitry, Valérie Nadeau, Yann Grobs, Renée Paradis, Nolwenn Samson, Ève Tremblay, Olivier Boucherat, Jolyane Meloche, Sébastien Bonnet, Steeve Provencher, François Potus, Roxane Paulin
    Arteriosclerosis, Thrombosis, and Vascular Biology.2020; 40(3): 783.     CrossRef
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    Hui Liu, Cheng Chen, Dongshen Ma, Yubing Li, Qianqian Yin, Qing Li, Chenxi Xiang
    Journal of Cellular and Molecular Medicine.2020; 24(11): 6308.     CrossRef
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    Dong-Hyeon Ha, Ahrum Min, Seongyeong Kim, Hyemin Jang, So Hyeon Kim, Hee-Jun Kim, Han Suk Ryu, Ja-Lok Ku, Kyung-Hun Lee, Seock-Ah Im
    Scientific Reports.2020;[Epub]     CrossRef
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    Maiara Bernardes Marques, Michael González-Durruthy, Bruna Félix da Silva Nornberg, Bruno Rodrigues Oliveira, Daniela Volcan Almeida, Ana Paula de Souza Votto, Luis Fernando Marins
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  • 12,075 View
  • 363 Download
  • 16 Web of Science
  • 14 Crossref
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Everolimus Plus Ku0063794 Regimen Promotes Anticancer Effects against Hepatocellular Carcinoma Cells through the Paradoxical Inhibition of Autophagy
Sang Chul Lee, Kee-Hwan Kim, Ok-Hee Kim, Sang Kuon Lee, Ha-Eun Hong, Byung Jo Choi, Wonjun Jeong, Say-June Kim
Cancer Res Treat. 2018;50(3):1023-1038.   Published online November 9, 2017
DOI: https://doi.org/10.4143/crt.2017.085
AbstractAbstract PDFPubReaderePub
Purpose
Everolimus only inhibits mammalian target of rapamycin complex 1 (mTORC1), whereas Ku0063794 inhibits both mTORC1 and mTORC2. Although they have similar anticancer effects, their combination has a synergistic effect against hepatocellular carcinoma (HCC) cells. We aimed to determine the mechanism underlying the synergistic effects of everolimus and Ku0063794 associated with autophagy in HCC cells.
Materials and Methods
We compared the effects of everolimus and Ku0063794, individually or in combination, on both the in vitro and in vivo models of HCCs.
Results
HepG2 cells treated with both agents had significantly lower rates of cell proliferation and higher apoptosis than the individual monotherapies (p < 0.05). Autophagic studies consistently indicated that, unlike the monotherapies, the combination therapy significantly reduced autophagy (p < 0.05). Autophagic blockage directly promoted the pro-apoptotic effects of combination therapy, suggesting autophagy as the survival mechanism of HCC cells. Unlike the monotherapies, combination therapy showed the potential to inhibit sirtuin 1 (SIRT1), the positive regulator of autophagy. SIRT1 overexpression abrogated the autophagy-inhibiting and pro-apoptotic effects of combination therapy. In a nude mouse xenograft model, the shrinkage of tumors was more prominent in mice treated with combination therapy than in mice treated with the respective monotherapies (p < 0.05). The immunohistochemical and immunofluorescence stains of the tumor obtained from the xenograft model showed that combination therapy had the potential of reducing autophagy and promoting apoptosis.
Conclusion
The combination of everolimus and Ku0063794 potentiates anticancer effects on HCCs through a decrease in autophagy, which is prompted by SIRT1 downregulation.

Citations

Citations to this article as recorded by  
  • Water-soluble 4-(dimethylaminomethyl)heliomycin exerts greater antitumor effects than parental heliomycin by targeting the tNOX-SIRT1 axis and apoptosis in oral cancer cells
    Atikul Islam, Yu-Chun Chang, Xiao-Chi Chen, Chia-Wei Weng, Chien-Yu Chen, Che-Wei Wang, Mu-Kuan Chen, Alexander S Tikhomirov, Andrey E Shchekotikhin, Pin Ju Chueh
    eLife.2024;[Epub]     CrossRef
  • Water-soluble 4-(dimethylaminomethyl)heliomycin exerts greater antitumor effects than parental heliomycin by targeting the tNOX-SIRT1 axis and apoptosis in oral cancer cells
    Atikul Islam, Yu-Chun Chang, Xiao-Chi Chen, Chia-Wei Weng, Chien-Yu Chen, Che-Wei Wang, Mu-Kuan Chen, Alexander S Tikhomirov, Andrey E Shchekotikhin, Pin Ju Chueh
    eLife.2024;[Epub]     CrossRef
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    María Paula Ceballos, Ariel Darío Quiroga, Nicolás Francisco Palma
    Biochemical Pharmacology.2023; 212: 115573.     CrossRef
  • Potentiation of the Anticancer Effects by Combining Docetaxel with Ku-0063794 against Triple-Negative Breast Cancer Cells
    Ye-Won Jeon, Ok-Hee Kim, Jin Sun Shin, Ha Eun Hong, Cho Hee Kim, Say-June Kim
    Cancer Research and Treatment.2022; 54(1): 157.     CrossRef
  • Combining Everolimus and Ku0063794 Promotes Apoptosis of Hepatocellular Carcinoma Cells via Reduced Autophagy Resulting from Diminished Expression of miR-4790-3p
    Ho Choi, Jung Park, Ok-Hee Kim, Kee-Hwan Kim, Ha Hong, Haeyeon Seo, Say-June Kim
    International Journal of Molecular Sciences.2021; 22(6): 2859.     CrossRef
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    Marius Farcas, Andrei-Alexandru Gavrea, Diana Gulei, Calin Ionescu, Alexandru Irimie, Cristina S. Catana, Ioana Berindan-Neagoe
    Frontiers in Nutrition.2019;[Epub]     CrossRef
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    Andreas Kroh, Jeanette Walter, Herdit Schüler, Jochen Nolting, Roman Eickhoff, Daniel Heise, Ulf Peter Neumann, Thorsten Cramer, Tom Florian Ulmer, Athanassios Fragoulis
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  • 10,184 View
  • 200 Download
  • 7 Web of Science
  • 8 Crossref
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Studying the Effect of Downregulating Autophagy-Related Gene LC3 on TLR3 Apoptotic Pathway Mediated by dsRNA in Hepatocellular Carcinoma Cells
Guilan Wang, Maona Zhang, Yunlong Li, Jiaming Zhou, Li Chen
Cancer Res Treat. 2017;49(1):230-245.   Published online June 13, 2016
DOI: https://doi.org/10.4143/crt.2015.506
AbstractAbstract PDFPubReaderePub
Purpose
The purpose of this study is to examine the role of the double-stranded RNA (dsRNA) activated Toll–interleukin-1 receptor domain-containing adaptor inducing interferon β (TRIF) signal pathway in triggering apoptosis in hepatocellular carcinoma (HCC) cells.
Materials and Methods
First, siRNA targeted autophagy–related gene LC3 (pU6H1-LC3 siRNA and siLC3) and a dsRNA used as a Toll-like receptor 3 (TLR3) ligand was constructed and synthesized, respectively. Then, a human HCC cell line was transfected with dsRNA, siLC3, and cotransfected with siLC3 and dsRNA (siLC3+dsRNA), respectively. Finally, quantification real-time polymerase chain reaction, western blotting, and immunofluorescence staining were used in the HCC line (SMMC7721), and MTT assay, flow cytometry, terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling, and transmission electron microscopy were used in an HCC xenograft model of nude mice. Human umbilical vein endothelial cell tube forming assay, color Doppler ultrasonographic flow image examination, and CD34-positive microvessel density were used in vitro and in vivo.
Results
Compared with untreated cells, the protein and mRNA expression of TLR3 and TRIF was up-regulated, in order, siLC3+dsRNA, dsRNA, and siLC3. Expression of LC3 was obviously down-regulated and the autophagosomes were significantly decreased in siLC3+dsRNA and siLC3, whereas in dsRNA (p < 0.05). LC3 and TRIF colocation was observed in HepG2 cells. Decreased cell viability, increased apoptosis, decrease in xenograft tumor volume, and angiogenesis potential were also observed in order (p < 0.05).
Conclusion
Suppression of intracellular autophagy resulted in decreased degradation of TRIF protein, which can promote triggering of apoptosis by the TLR3-TRIF pathway. dsRNA and siLC3 could play anticancer roles in coordination.

Citations

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  • A Multi-Omics Analysis of a Mitophagy-Related Signature in Pan-Cancer
    Nora Agir, Ilias Georgakopoulos-Soares, Apostolos Zaravinos
    International Journal of Molecular Sciences.2025; 26(2): 448.     CrossRef
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    Lin Shi, Zhaozhong Xu, Gang Wu, Xiaoting Chen, Yuanyuan Huang, Yanjing Wang, Weiqiang Jiang, Bin Ke
    BMC Cancer.2017;[Epub]     CrossRef
  • 14,406 View
  • 181 Download
  • 8 Web of Science
  • 5 Crossref
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Blockade of Autophagy Aggravates Endoplasmic Reticulum Stress and Improves Paclitaxel Cytotoxicity in Human Cervical Cancer Cells
Li Xu, Jing-Hua Liu, Jing Zhang, Na Zhang, Zan-Hong Wang
Cancer Res Treat. 2015;47(2):313-321.   Published online September 11, 2014
DOI: https://doi.org/10.4143/crt.2013.222
AbstractAbstract PDFPubReaderePub
Purpose
Autophagy is one of the ways to degrade unfolded proteins after endoplasmic reticulum (ER) stress. The purpose of this study is to determine whether a blockade of autophagy leads to aggravated endoplasmic reticulum stress, which then induces cells apoptosis in HeLa cells treated with paclitaxel.
Materials and Methods
Autophagy activation and the proapoptotic effects were characterized using monodansylcadaverine labeling and Hoechest staining, respectively. A Western blot analysis was used to detect the expression of apoptotic and autophagy-related genes. A flow cytometry was used to assess the cell apoptosis ratio.
Results
Paclitaxel exposure induced the aggregation of autophagosomes in the cytoplasms of cervical cancer HeLa cells. The expression of Beclin 1 and LC3 II were upregulated, but p62 was downregulated, which suggests that autophagy was promoted by paclitaxel. On the other hand, the expression of GRP78 obviously increased, suggesting that ER stress was induced after paclitaxel treatment. The cell proliferation assay indicated that a knockdown of Beclin 1 sensitized HeLa cells to paclitaxel. Furthermore, paclitaxel-mediated apoptotic cell death was further potentiated by the pretreatment with autophagy inhibitor chloroquine or small interfering RNA against Beclin 1. These results suggest that an induction of autophagy by paclitaxel may induce cell survival rather than cell death in HeLa cells; moreover, inhibition of autophagy led to an aggravated ER stress and an induction of downstream apoptosis.
Conclusion
Our results reveal autophagy induced by paclitaxel conferred protection of tumor cells against apoptosis, and blockade of autophagy subsequently aggravated ER stress, enhancing the apoptosis associated with paclitaxel treatment in HeLa cells.

Citations

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  • Endoplasmic reticulum stress induced autophagy in cancer and its potential interactions with apoptosis and ferroptosis
    Haitang Liao, Shuang Liu, Qiang Ma, He Huang, Arul Goel, Pedram Torabian, Chakrabhavi Dhananjaya Mohan, Chenyang Duan
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Radiation-Induced Autophagy Contributes to Cell Death and Induces Apoptosis Partly in Malignant Glioma Cells
Guk Heui Jo, Oliver Bögler, Yong-Joon Chwae, Heon Yoo, Seung Hoon Lee, Jong Bae Park, Youn-Jae Kim, Jong Heon Kim, Ho-Shin Gwak
Cancer Res Treat. 2015;47(2):221-241.   Published online August 29, 2014
DOI: https://doi.org/10.4143/crt.2013.159
AbstractAbstract PDFPubReaderePub
Purpose
Radiation-induced autophagy has been shown to play two different roles, in malignant glioma (MG) cells, cytocidal or cytoprotective. However, neither the role of radiation-induced autophagy for cell death nor the existence of autophagy-induced apoptosis, a well-known cell-death pathway after irradiation, has been verified yet. Materials and Methods We observed both temporal and dose-dependent response patterns of autophagy and apoptosis to radiation in MG cell lines. Additionally, we investigated the role of autophagy in apoptosis through knockdown of autophagy-related proteins. Results Autophagic activity measured by staining of acidic vesicle organelles and Western blotting of LC-3 protein increased in proportion to radiation dose from day 1 to 5 after irradiation. Apoptosis measured by annexin-V staining and Western blotting of cleaved poly(ADP-ribose) polymerase demonstrated relatively late appearance 3 days after irradiation that increased for up to 7 days. Blocking of pan-caspase (Z-VAD-FMK) did not affect apoptosis after irradiation, but silencing of Atg5 effectively reduced radiation-induced autophagy, which decreased apoptosis significantly. Inhibition of autophagy in Atg5 knockdown cells was shown to be beneficial for cell survival. Stable transfection of GFP-LC3 cells was observed after irradiation. Annexin-V was localized in cells bearing GFP-LC3 punctuated spots, indicating autophagy in immunofluorescence. Some of these punctuated GFP-LC3 bearing cells formed conglomerated spots and died in final phase. Conclusion These findings suggest that autophagy appears earlier than apoptosis after irradiation and that a portion of the apoptotic population that appears later is autophagy-dependent. Thus, autophagy is a pathway to cell death after irradiation of MG cells.

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