ArticleBJC reports2025
Tumor cell-intrinsic PD-1 regulates chemotherapy resistance in colorectal cancer cells by activating downstream MAPK signaling.
Article in BJC reports, 2025. 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
5 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) remains a significant clinical challenge. Immunotherapy against programmed cell death 1 protein (PD-1) in CRC has limited success. Intriguingly, CRC cells express PD-1 (ciPD-1) intrinsically, and we report here its function with respect to chemotherapy.
methodsWe evaluated the associations between ciPD-1 expression and disease progression, overall survival, and upregulation of survival pathways in human CRC tumors. Expression levels of ciPD-1 in CRC cells were modulated to evaluate its biological role in vitro.
resultsHigh expression levels of PD-1 in CRC tumors are associated with inferior outcomes; these tumors are also more aggressive and drug-resistant. Expression levels of ciPD-1 in CRC cells increase during 5-FU or CPT-11 treatment and are accompanied by upregulation of cell survival pathways. When ciPD-1 is inhibited, the cell-killing effects of 5-FU or CPT-11 were significantly increased. Our data show that ciPD-1 signaling occurs via MAPK signaling in CRC cells to support survival under stress conditions.
conclusionsCRC tumors with high levels of ciPD-1 are more aggressive and associated with inferior outcomes. Reducing ciPD-1 levels in CRC cells make them more sensitive to chemotherapy. The aggregate results suggest that using a PD-1 inhibitor with first-line treatments in CRC could improve therapeutic efficacy. Proposed biological role of ciPD-1 in CRC cells. After exposure to chemotherapy, radiotherapy, or nutrient deprivation, ciPD-1 expression is elevated in CRC cells. Subsequently, ciPD-1 activates MAPK and AKT signaling pathways to increase proliferation and differentiation, resulting in drug resistance and tumor growth in CRC cells. The administration of anti-PD-1 immunotherapy with chemotherapy in CRC cells could abrogate ciPD-1 activity and enhance the efficacy of chemotherapy to overcome resistance.
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.