ArticleOncology letters2018
Autophagy activation promotes bevacizumab resistance in glioblastoma by suppressing Akt/mTOR signaling pathway.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Targeting autophagy for combating chemoresistance and radioresistance in glioblastoma.Apoptosis : an international journal on programmed cell death · 2018Pooled it
- The CHI3L1 protein plays role as a protecting factor against autophagy in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2026Article
- The Time-Dependent Effects of Temozolomide on Autophagy Gene Expression in Glioblastoma Cells.Biomedicines · 2026Article
- Exploring the efficacy of a novel cannabidiol and bevacizumab combination in non-small cell lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Liposomal honokiol enhance the anti-tumor effect of bevacizumab in glioblastoma by inhibiting autophagy.Future science OA · 2025Article
- Epigenetic Alterations in Glioblastoma Multiforme as Novel Therapeutic Targets: A Scoping Review.International journal of molecular sciences · 2025Article
- Autophagy in brain tumors: molecular mechanisms, challenges, and therapeutic opportunities.Journal of translational medicine · 2025Review
- Role of Autophagy and AMPK in Cancer Stem Cells: Therapeutic Opportunities and Obstacles in Cancer.International journal of molecular sciences · 2024Review
- Basic Fibroblast Growth Factor Accumulation in Culture Medium Masks the Direct Antitumor Effect of Anti-VEGF Agent Bevacizumab.Doklady. Biochemistry and biophysics · 2024Article
- ID1Cell death & disease · 2024Article
- New Salicylanilide Derivatives and Their Peptide Conjugates as Anticancer Compounds: Synthesis, Characterization, andACS omega · 2024Article
- Direct antitumor activity of bevacizumab: an overlooked mechanism?Frontiers in pharmacology · 2024Article
- Developing a dual VEGF/PDL1 inhibitor based on high-affinity scFv heterodimers as an anti-cancer therapeutic strategy.Scientific reports · 2023Article
- Pyroptosis, ferroptosis, and autophagy cross-talk in glioblastoma opens up new avenues for glioblastoma treatment.Cell communication and signaling : CCS · 2023Review
- Review
- Re-Sensitizing Cancer Stem Cells to Conventional Chemotherapy Agents.International journal of molecular sciences · 2023Review
- Inhibition of autophagy; an opportunity for the treatment of cancer resistance.Frontiers in cell and developmental biology · 2023Review
- Exosomal miR-93-5p regulated the progression of osteoarthritis by targeting ADAMTS9.Open medicine (Warsaw, Poland) · 2023Article
- Enhancing Anti-Cancer Therapy with Selective Autophagy Inhibitors by Targeting Protective Autophagy.Biomolecules & therapeutics · 2023Review
- Biologic Functions of Hydroxychloroquine in Disease: From COVID-19 to Cancer.Pharmaceutics · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas are the most common primary and malignant brain tumors. The standard therapy includes surgery and radiotherapy plus chemotherapy, with additional bevacizumab to block the angiogenesis in tumors. However, the ever-growing tolerance of glioblastomas to chemotherapeutic drugs impairs the clinical outputs of tumor treatment. The present study investigated the tolerance of glioblastomas to bevacizumab. Although bevacizumab resulted in direct anti-proliferation and pro-apoptosis effects on glioblastoma cells via downregulating the anti-apoptotic proteins and upregulating the pro-apoptotic proteins, tolerance was also encountered that was mainly caused by autophagy induction in tumor cells. The suppressed Akt-mTOR signaling pathway led to the upregulated autophagy process. Blockade of the autophagy process significantly increased the tumor-suppressive effect of bevacizumab on glioblastoma cells. To our knowledge, the present study is the first to report the involvement of autophagy in the tolerance of glioblastomas to bevacizumab. Therefore, autophagy inhibition may be considered a novel way to overcome the tolerance of glioblastomas to anti-angiogenic agents.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.