ArticleNPJ breast cancer2021
RIPK1 is a negative mediator in Aquaporin 1-driven triple-negative breast carcinoma progression and metastasis.
Article in NPJ breast cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- miR-3921 functions as a tumor suppressor and negatively regulates RIPK1 in gastric cancer.PeerJ · 2026Article
- Lysosomal-stress-driven cargo-fate switching between autophagic degradation and small extracellular vesicle release in triple-negative breast cancer: a hypothesis and theory article.Frontiers in oncology · 2026Article
- Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Cracking the code of cancer immunotherapy resistance: emerging roles of pyroptosis and necroptosis.Journal of experimental & clinical cancer research : CR · 2025Review
- The comprehensive potential of AQP1 as a tumor biomarker: evidence from kidney neoplasm cohorts, cell experiments and pan-cancer analysis.Human genomics · 2025Article
- AQP1 Affects Necroptosis by Targeting RIPK1 in Endothelial Cells of Atherosclerosis.Vascular health and risk management · 2025Article
- Targeting TNFR1-driven necroptosis in breast cancer.EXCLI journal · 2025Review
- Identification of EMT-associated prognostic features among grade II/III gliomas.Scientific reports · 2024Article
- The Involvement of Peroxiporins and Antioxidant Transcription Factors in Breast Cancer Therapy Resistance.Cancers · 2023Review
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Disintegrin-like Protein Strategy to Inhibit Aggressive Triple-Negative Breast Cancer.International journal of molecular sciences · 2023Article
- RIPK1 is aberrantly expressed in multiple B-cell cancers and implicated in the underlying pathogenesis.Discover oncology · 2023Article
- The roles of long non-coding RNAs in the necroptotic signaling of colon cancer cells.Molecular biology reports · 2023Article
- Aquaporins in Skin.Advances in experimental medicine and biology · 2023Article
- Role of Receptor Interacting Protein (RIP) kinases in cancer.Genes & diseases · 2022Review
- Immunotherapy landscape analyses of necroptosis characteristics for breast cancer patients.Journal of translational medicine · 2022Article
- Targeting regulated cell death (RCD) with small-molecule compounds in triple-negative breast cancer: a revisited perspective from molecular mechanisms to targeted therapies.Journal of hematology & oncology · 2022Review
- RIPK1 is a negative mediator in Aquaporin 1-driven triple-negative breast carcinoma progression and metastasis.NPJ breast cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The triple-negative breast carcinoma (TNBC) is the most aggressive subtype of breast cancer. In TNBC, Aquaporin 1 (AQP1), a water-transporting transmembrane protein, is aberrantly enriched in cytoplasm and causes tumor cell death evasion. However, the carcinogenetic bioactivities of cytoplasmic AQP1 cannot be attributed to the canonical "osmotic engine model". In the present study, the receptor-interacting protein kinase 1 (RIPK1), a cell death regulator, was identified to negatively mediate AQP1-driven TNBC progression and metastasis. AQP1 overabundance and RIPK1 depletion occurred in TNBC, which were correlated with aggressive oncological features and poor prognosis. AQP1 bound with RIPK1, resulting in the inhibition of RIPK1/RIPK3/MLKL-mediated necroptosis and RIPK1/caspase-8/caspase-3-mediated apoptosis. Genetic inhibition of RIPK1 significantly exacerbated the pro-tumor effect of AQP1, while ectopic expression of RIPK1 notably blunted AQP1 signaling. Mechanistically, AQP1 binds to the D324 site of RIPK1, and facilitates RIPK1 cleavage and inactivation by excessively activating the caspase-8/RIPK1 negative feedback loop. RIPK1
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.