ArticleAutophagy2010
Roles of autophagy in cetuximab-mediated cancer therapy against EGFR.
Article in Autophagy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 89 citations in OpenAlex.
- Autophagy induced by metabolic processes leads to solid tumor cell metastatic dormancy and recurrence.Medical oncology (Northwood, London, England) · 2025Review
- Cetuximab-based PROteolysis targeting chimera for effectual downregulation of NSCLC with varied EGFR mutations.International journal of biological macromolecules · 2023Article
- Fundamental concepts of protein therapeutics and spacing in oncology: an updated comprehensive review.Medical oncology (Northwood, London, England) · 2023Review
- Clinical Trials for Oral, Inhaled and Intravenous Drug Delivery System for Lung Cancer and Emerging Nanomedicine-Based Approaches.International journal of nanomedicine · 2023Review
- Article
- Autophagy awakens-the myriad roles of autophagy in head and neck cancer development and therapeutic response.Molecular carcinogenesis · 2022Review
- Review
- Article
- Prolonged cetuximab treatment promotes p27Scientific reports · 2021Article
- Role of PARP1-mediated autophagy in EGFR-TKI resistance in non-small cell lung cancer.Scientific reports · 2020Article
- Molecular Insights into the Multifunctional Role of Natural Compounds: Autophagy Modulation and Cancer Prevention.Biomedicines · 2020Review
- Adaptive response of resistant cancer cells to chemotherapy.Cancer biology & medicine · 2020Review
- Role of Autophagy in Cancer Cell Response to Nucleolar and Endoplasmic Reticulum Stress.International journal of molecular sciences · 2020Review
- PPARδ is a regulator of autophagy by its phosphorylation.Oncogene · 2020Article
- The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity.Frontiers in oncology · 2020Review
- Torin2 inhibits the EGFR-TKI resistant Non-Small Lung Cancer cell proliferation through negative feedback regulation of Akt/mTOR signaling.Journal of Cancer · 2020Article
- Review
- Review
- Drug repurposing to overcome resistance to various therapies for colorectal cancer.Cellular and molecular life sciences : CMLS · 2019Review
- Predictive and prognostic implications of 4E-BP1, Beclin-1, and LC3 for cetuximab treatment combined with chemotherapy in advanced colorectal cancer with wild-type KRAS: Analysis from real-world data.World journal of gastroenterology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cetuximab is an epidermal growth factor receptor (EGFR)-blocking antibody that is approved to treat several types of solid cancers in patients. We recently showed that cetuximab can induce autophagy in cancer cells by both inhibiting the class I phosphatidylinositol 3-kinase (PtdIns3K)/Akt/mammalian target of rapamycin (mTOR) pathway and activating the class III PtdIns3K (hVps34)/beclin 1 pathway. In the current study, we investigated the relationship between cetuximab-induced autophagy and apoptosis and the biological roles of autophagy in cetuximab-mediated cancer therapy. We found that cetuximab induced autophagy in cancer cells that show strong or weak induction of apoptosis after cetuximab treatment but not in those that show only cytostatic growth inhibition. Inhibition of cetuximab-induced apoptosis by a caspase inhibitor prevented the induction of autophagy. Conversely, inhibition of cetuximab-induced autophagy by silencing the expression of autophagy-related genes (Atg) or treating the cancer cells with lysosomal inhibitors enhanced the cetuximab-induced apoptosis, suggesting that autophagy was a protective cellular response to cetuximab treatment. On the other hand, cotreatment of cancer cells with cetuximab and the mTOR inhibitor rapamycin resulted in an Atg-dependent and lysosomal inhibition-sensitive death of cancer cells that show only growth inhibition or weak apoptosis after cetuximab treatment, indicating that cell death may be achieved by activating the autophagy pathway in these cells. Together, our findings may guide the development of novel clinical strategies for sensitizing cancer cells to EGFR-targeted therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.