Article
Cell Biology
Delong Yin, Guoqing Jin, Hong He, Wei Zhou, Zhenbo Fan, Chen Gong, Jing Zhao, Huihua Xiong
Summary: Celecoxib has shown to enhance the sensitivity of GBM cells to TMZ in chemotherapy by inhibiting cell proliferation, increasing apoptosis, and autophagy. The potential molecular mechanisms are related to mitochondrial metabolism and respiratory chain inhibition.
Article
Cell Biology
Denise Sighel, Michela Notarangelo, Shintaro Aibara, Angela Re, Gianluca Ricci, Marianna Guida, Alessia Soldano, Valentina Adami, Chiara Ambrosini, Francesca Broso, Emanuele Filiberto Rosatti, Sara Longhi, Mariachiara Buccarelli, Quintino G. D'Alessandris, Stefano Giannetti, Simone Pacioni, Lucia Ricci-Vitiani, Joanna Rorbach, Roberto Pallini, Sandrine Roulland, Alexey Amunts, Ines Mancini, Angelika Modelska, Alessandro Quattrone
Summary: This study suggests that targeting mitochondrial translation could be a potential therapeutic strategy to suppress GSC growth in GBM. The bacterial antibiotic quinupristin/dalfopristin (Q/D) was found to effectively inhibit GSC growth by binding to the large mitoribosomal subunit, inhibiting mitochondrial protein synthesis, and disrupting OXPHOS complexes.
Article
Oncology
Chia-Hung Chien, Wen-Bin Yang, Jian-Ying Chuang, Jung-Shun Lee, Wei-An Liao, Chih-Yuan Huang, Pin-Yuan Chen, An-Chih Wu, Shun-Tai Yang, Chien-Cheng Lai, Pei- Chi, Jui-Mei Chu, Siao Muk Cheng, Chan-Chuan Liu, Daw-Yang Hwang, Shang-Hung Chen, Kwang-Yu Chang
Summary: This study demonstrates that SH3GLB1 promotes resistance to temozolomide through autophagy-mediated alteration of mitochondrial function in glioblastoma.
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Ji-Young Yoo, Margaret Yeh, Yin-Ying Wang, Christina Oh, Zhong-Ming Zhao, Balveen Kaur, Tae-Jin Lee
Summary: The study demonstrated that overexpression of miR-138 sensitizes GBM cells to TMZ treatment and increases apoptotic cell death. Mechanistically, miR-138 directly repressed Survivin expression to enhance apoptosis induced by TMZ.
Article
Chemistry, Multidisciplinary
Munki Choo, Van-Hieu Mai, Han Sun Kim, Dong-Hwa Kim, Ja-Lok Ku, Sang Kook Lee, Chul-Kee Park, Yong Jin An, Sunghyouk Park
Summary: The study investigated the relationship among TMZ-resistance, cell shape, and lipid metabolism in GBM cells. The study found distinct differences in cell shapes between TMZ-sensitive and resistant cells, as well as increased cholesterol and fatty acid synthesis, and lower lipid unsaturation in the resistant cells. Transcriptomic analysis showed upregulation of lipid synthesis pathways in the resistant cells. Inhibition of lipid pathways showed stronger effects on resistant cells. The study suggests a ternary relationship among cell shape, lipid composition, and TMZ-resistance, and identifies SREBP and fatostatin as promising targets for drug-resistant glioblastoma.
ACTA PHARMACOLOGICA SINICA
(2023)
Article
Medicine, Research & Experimental
Eryan Yang, Lin Wang, Weili Jin, Xing Liu, Qixue Wang, Ye Wu, Yanli Tan, Yunfei Wang, Xiaoteng Cui, Jixing Zhao, Fei Tong, Biao Hong, Menglin Xiao, Xiaomin Liu, Chuan Fang, Chunsheng Kang
Summary: This study highlights the importance of PTRF in glioblastoma and its role as a predictor of prognosis in GBM patients treated with temozolomide. It also identifies a novel mechanism contributing to temozolomide resistance. Furthermore, this study provides a new idea for GBM therapy.
Article
Oncology
Jian Yu, Ge Gao, Xiangpin Wei, Yang Wang
Summary: This study revealed that TTK protein kinase promotes TMZ resistance in GBM cells by inducing autophagy both in vitro and in vivo. TTK inhibitors significantly inhibited GBM cell proliferation and enhanced the growth-suppressive effect of TMZ. Furthermore, blocking TTK could suppress the autophagy process in GBM cells.
Article
Cell Biology
Fan Yang, Duo Zhang, Haowen Jiang, Jiangbin Ye, Lin Zhang, Stephen J. Bagley, Jeffery Winkler, Yanqing Gong, Yi Fan
Summary: A compound called toosendanin (TSN) has been found to reprogram macrophages in order to enhance the immune response against glioblastoma (GBM) in mouse models. This compound reverses macrophage-mediated tumor immunosuppression, leading to increased T cell infiltration and activation, and reduced exhaustion.
SCIENCE TRANSLATIONAL MEDICINE
(2023)
Article
Multidisciplinary Sciences
Yufei Lan, Tao Yang, Qu Yue, Zhao Wang, Xiangyang Zhong, Xin Luo, Boming Zuo, Manqing Zhang, Tianci Zeng, Boyang Liu, Hongbo Guo
Summary: This study demonstrated, for the first time, that amplifying IRP1 signals can reverse TMZ resistance and suppress tumor growth in vivo by inhibiting NFKB2 in the noncanonical NF-kappa B signaling pathway. Additionally, we identified that NFKB2 affects the TMZ sensitivity of GBM by modulating the expression of LCN2 and FPN1. In conclusion, this study reveals the role of the IRP1/NFKB2 pathway in regulating the LCN2/FPN1 signaling axis during the progression of TMZ resistance, suggesting a potential innovative therapeutic strategy for GBM.
Article
Biochemistry & Molecular Biology
Luca X. Zampieri, Martina Sboarina, Andrea Cacace, Debora Grasso, Leopold Thabault, Loic Hamelin, Thibaut Vazeille, Elodie Dumon, Rodrigue Rossignol, Raphael Frederick, Etienne Sonveaux, Florence Lefranc, Pierre Sonveaux
Summary: The study found that mitochondria in glioblastoma cells become fitter in response to chemotherapy, leading to chemoresistance. By inhibiting oxidative phosphorylation and/or autophagy/mitophagy, this resistance can be targeted. Some PARP inhibitors were also found to be inhibitors of mitochondrial Complex I.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Cell Biology
Yu-Ting Tsai, Wei-Lun Lo, Pin-Yuan Chen, Chiung-Yuan Ko, Jian-Ying Chuang, Tzu-Jen Kao, Wen-Bing Yang, Kwang-Yu Chang, Chia-Yang Hung, Ushio Kikkawa, Wen-Chang Chang, Tsung- Hsu
Summary: Sp1-regulated PGE2 production activates FAO and TCA cycle in mitochondria, resulting in TMZ resistance in GBM. These findings provide a new strategy to attenuate drug resistance or to re-sensitize recurrent GBM.
JOURNAL OF BIOMEDICAL SCIENCE
(2022)
Article
Biochemistry & Molecular Biology
Hong-Yi Lin, Kuo-Hsing Liao, Chiung-Yuan Ko, Guan-Yuan Chen, Sung-Po Hsu, Chia-Yang Hung, Tsung- Hsu
Summary: The study suggests that 17β-estradiol plays a crucial role in the development of drug resistance in glioblastoma multiforme (GBM) by reducing oxidative stress and inducing drug resistance through NRF2 expression.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Chemistry, Medicinal
Yang Wang, Ge Gao, Xiangpin Wei, Yang Zhang, Jian Yu
Summary: UBE2T plays a crucial role in mediating resistance of glioblastoma cells to temozolomide (TMZ) treatment by regulating the Wnt/I3-catenin signaling pathway. Inhibition of UBE2T sensitizes GBM cells to TMZ, while UBE2T overexpression promotes TMZ resistance. Targeting UBE2T may be a potential strategy to overcome TMZ resistance in GBM.
DRUG DESIGN DEVELOPMENT AND THERAPY
(2023)
Article
Biochemistry & Molecular Biology
Huaijin Zhang, Yuling Chen, Xiaohui Liu, Haiteng Deng
Summary: This study found that mitochondrial dysfunction, rotenone treatment, elevated Ca2+ levels, and activation of the JNK-STAT3 pathway all contribute to increased resistance of glioblastoma to TMZ. Inhibiting JNK or STAT3 can increase sensitivity to TMZ. Co-administration of TMZ with a JNK or STAT3 inhibitor holds promise as an effective treatment for glioblastoma.
Article
Medicine, General & Internal
Hina Ahsan, Shaukat Iqbal Malik, Fawad Ali Shah, Hamed A. El-Serehy, Amin Ullah, Zafar Abbas Shah
Summary: This study investigates the expression profiling of NF-kappa B p65 (RelA) and TNF alpha, as well as the effectiveness of Celecoxib in combination with Temozolomide in reducing the growth of human GBM cell line SF-767. The results demonstrate that Celecoxib reduces cell viability, cell proliferation, and the expression of NF-kappa B p65 (RelA) and TNF alpha in a dose-dependent manner. These findings suggest that Celecoxib therapy could mitigate the invasive characteristics of GBM cells by inhibiting the inflammatory cascade mediated by NF-kappa B.
JOURNAL OF CLINICAL MEDICINE
(2023)
