ArticleScientific reports2026
Tumor-derived type IX collagen regulates dormancy in triple-negative breast cancer cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Metastasis and recurrence of triple-negative breast cancer (TNBC), are mainly attributed to the presence of dormant cancer cells (DCCs), yet the molecular mechanisms governing the maintenance and reactivation of DCC dormancy remain poorly elucidated. This study identified collagen IX alpha 1 chain (Col9a1) as a gene specifically expressed in TNBC dormant cells and confirmed that it is a key molecule sustaining DCC dormancy. Mechanistic studies revealed that COL9A1 sustains TNBC cell dormancy by suppressing the FAK-AKT-p27 signaling axis, thereby inducing G0/G1 cell cycle arrest. Col9a1 knockdown reactivates DCCs, and the reactivated cells recruit natural killer (NK) cells by upregulating retinoic acid early inducible 1γ (RAE-1γ) and secreting proinflammatory cytokines (IL-15/IL-18), thus abrogating the immune evasion capacity of DCCs and enhancing the chemosensitivity of reactivated TNBC cells to docetaxel. This study uncovers a novel mechanism by which COL9A1 regulates TNBC cell dormancy, indicating that COL9A1 can serve as a potential biomarker for assessing the dormant phenotype of TNBC and predicting tumor recurrence, as well as a novel therapeutic target for TNBC. This study also provides preclinical evidence for developing COL9A1-targeted combination therapies for TNBC.
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.