ArticleCancer cell international2024
Lysosomal gene ATP6AP1 promotes doxorubicin resistance via up-regulating autophagic flux in breast cancer.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- [ATPase HZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Magnolin overcomes EGFR TKI resistance in NSCLC by modulation of NDRG1-NRG2-HECW1 pathway.Acta pharmacologica Sinica · 2026Article
- Breast cancer: taxonomy, distribution analysis, risk factors, predictive biomarkers, and modern treatment method.Apoptosis : an international journal on programmed cell death · 2026Review
- Autophagy in doxorubicin resistance: basic concepts, therapeutic perspectives and clinical translation.Frontiers in immunology · 2025Review
- Development of a Novel Lysosomal Gene-based Prognostic Panel and Uncovering EIF4EBP1 as a Biomarker for Breast Cancer.Current genomics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundBreast cancer remains the most prevalent malignancy in women. Chemotherapy is the primary systemic treatment modality, and the effectiveness of treatment is often hampered by chemoresistance. Autophagy has been implicated in promoting chemoresistance, as elevated autophagic flux supports tumor cell survival under therapeutic stress. Since lysosomes are essential for the completion of autophagy, their role in autophagy-related chemoresistance has been insufficiently studied. This study aims to elucidate the role of the lysosomal gene ATP6AP1 in promoting chemoresistance in breast cancer by upregulating autophagic flux.
methodsDoxorubicin-induced cell death was assessed by cytotoxicity, flow cytometry, lactate dehydrogenase (LDH) release assays in various breast cancer cell lines. Autophagic flux was assessed with western blot and the mRFP-GFP-LC3 fluorescence imaging. Breast cancer cells were infected with shRNA lentivirus targeting ATP6AP1, allowing investigation its tole in doxorubicin-induced cell death. ATP6AP1 expression and its association with prognosis were evaluated using public databases and immunohistochemistry.
resultsDoxorubicin-induced cell death in breast cancer cells is negatively correlated with increased autophagic flux and lysosomal acidification. The lysosomal gene ATP6AP1, which plays a role in autophagic processes, is upregulated in breast cancer tissues. Knocking down ATP6AP1 reduces autophagy-mediated doxorubicin resistance by inhibiting autophagic flux and lysosomal acidification in breast cancer cells. Data analysis from public databases and our cohort indicate that elevated ATP6AP1 expression correlates with poor response to doxorubicin-based neoadjuvant chemotherapy (NAC) and worse prognosis.
conclusionsDoxorubicin-induced cytotoxicity is associated with autophagy flux in breast cancer. The lysosomal gene ATP6AP1 facilitates autolysosome acidification and contributes to doxorubicin resistance in breast cancer.
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.