ArticleJournal of thoracic disease2026
Yifei Sanjie Formula in improving the response to PD-1 blockade by lung cancer through the attenuation of the USP7-NR1H4-bile acid metabolism axis.
Article in Journal of thoracic disease, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Yifei Sanjie Formula (YFSJF), a traditional Chinese medicine (TCM) formulation, has been clinically observed to enhance the efficacy of programmed cell death protein 1 (PD-1) blockade in patients with advanced lung adenocarcinoma. However, the underlying mechanisms of its effect remain unclear. This study aimed to clarify the molecular mechanism by which YFSJF enhances the efficacy of PD-1 inhibitors, with a focus on its role in regulating the ubiquitin-specific protease 7 (USP7)-nuclear receptor subfamily 1 group H member 4 (NR1H4)-bile acid metabolism axis. Methods: Using Results: YFSJF significantly inhibited the proliferation, migration, and invasion of lung cancer cells while enhancing the antitumor efficacy of PD-1 blockade by modulating immune responses. USP7 was found to be highly expressed in lung cancer tissues and was associated with poor prognosis. We further found that YFSJF promoted the ubiquitin-mediated degradation of NR1H4 by downregulating USP7, thereby altering the levels of bile acid metabolites such as taurochenodeoxycholic acid (TCDCA) and glycocholic acid (GCA). USP7 knockdown impaired NR1H4 stability via the ubiquitin-proteasome pathway, influencing bile acid metabolism and immune-related pathways. Conclusions: YFSJF regulates bile acid metabolism reprogramming through the USP7-NR1H4-bile acid metabolism axis to affect immune-related pathways and enhance the efficacy of PD-1 inhibitors. These findings provide insights into the mechanisms underlying the immunomodulatory role of YFSJF and support its use as a complement to immunotherapy in lung cancer treatment.
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.