ArticleOncotarget2016
Identification of breast cancer cell subtypes sensitive to ATG4B inhibition.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 72 citations in OpenAlex.
- ATG4B is required for mTORC1-mediated anabolic activity and is associated with clinical outcomes in non-small cell lung cancer.FEBS open bio · 2026Article
- Energy Deficiency-Induced ATG4B Nuclear Translocation Inhibits PRMT1-Mediated DNA Repair and Promotes Leukemia Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Autophagy Protease ATG4D Facilitates Proliferation and Malignancy of Osteosarcoma Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Upregulated ATG4B predicts poor prognosis and correlates with angiogenesis in osteosarcoma.Journal of the Egyptian National Cancer Institute · 2025Article
- Evaluation of autophagy related ATG4B gene, protein and miR-655-3p expression levels in endometrial cancer and hyperplasia.Journal of gynecologic oncology · 2025Article
- Natural autophagy modulators in non-communicable diseases: from autophagy mechanisms to therapeutic potential.Acta pharmacologica Sinica · 2025Review
- Targeting GABARAPL1/HIF-2a axis to induce tumor cell apoptosis in nasopharyngeal carcinoma.Iranian journal of basic medical sciences · 2024Article
- Forkhead Box Q1 is a novel regulator of autophagy in breast cancer cells.Molecular carcinogenesis · 2023Article
- Loss of ATG4B and ATG4A results in two-stage cell cycle defects in pancreatic ductal adenocarcinoma cells.Journal of cell science · 2023Article
- Construction and validation of a prognostic model based on autophagy-related genes for hepatocellular carcinoma in the Asian population.BMC genomics · 2023Article
- The mammalian Sterile 20-like kinase 4 (MST4) signaling in tumor progression: Implications for therapy.Cancer letters · 2023Review
- ATG4B and pS383/392-ATG4B serve as potential biomarkers and therapeutic targets of colorectal cancer.Cancer cell international · 2023Article
- Discovery and mechanism studies of a novel ATG4B inhibitor Ebselen by drug repurposing and its anti-colorectal cancer effects in mice.Cell & bioscience · 2022Article
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- Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance.Molecular and cellular biochemistry · 2022Review
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- Proteomics-derived basal biomarker DNA-PKcs is associated with intrinsic subtype and long-term clinical outcomes in breast cancer.NPJ breast cancer · 2021Article
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- ATG4B Inhibitor UAMC-2526 Potentiates the Chemotherapeutic Effect of Gemcitabine in a Panc02 Mouse Model of Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy, a lysosome-mediated degradation and recycling process, functions in advanced malignancies to promote cancer cell survival and contribute to cancer progression and drug resistance. While various autophagy inhibition strategies are under investigation for cancer treatment, corresponding patient selection criteria for these autophagy inhibitors need to be developed. Due to its central roles in the autophagy process, the cysteine protease ATG4B is one of the autophagy proteins being pursued as a potential therapeutic target. In this study, we investigated the expression of ATG4B in breast cancer, a heterogeneous disease comprised of several molecular subtypes. We examined a panel of breast cancer cell lines, xenograft tumors, and breast cancer patient specimens for the protein expression of ATG4B, and found a positive association between HER2 and ATG4B protein expression. We showed that HER2-positive cells, but not HER2-negative breast cancer cells, require ATG4B to survive under stress. In HER2-positive cells, cytoprotective autophagy was dependent on ATG4B under both starvation and HER2 inhibition conditions. Combined knockdown of ATG4B and HER2 by siRNA resulted in a significant decrease in cell viability, and the combination of ATG4B knockdown with trastuzumab resulted in a greater reduction in cell viability compared to trastuzumab treatment alone, in both trastuzumab-sensitive and -resistant HER2 overexpressing breast cancer cells. Together these results demonstrate a novel association of ATG4B positive expression with HER2 positive breast cancers and indicate that this subtype is suitable for emerging ATG4B inhibition strategies.
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