ArticleCell death & disease2026
ΔNp63α drives serine synthesis to promote carboplatin resistance in NSCLC.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Association between the TP63 and CIR1 polymorphisms and non-small cell lung cancer in Chinese population.Journal of cardiothoracic surgery · 2026Article
- TRIM29 suppresses malignant progression in lung squamous cell carcinoma by shaping an immunosuppressive tumor microenvironment.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serine metabolism is a critical vulnerability in cancer; however, its role in mediating therapeutic resistance in non-small cell lung cancer (NSCLC) remains incompletely understood. In this study, we identify key enzymes in the serine synthesis pathway (SSP), namely PHGDH, PSAT1 and PSPH, as well as the serine transporter SLC1A4, which are significantly overexpressed in lung cancer and correlate with poor patient prognosis. We show that serine contributes to carboplatin resistance in NSCLC, particularly in lung squamous cell carcinoma (LUSC). Notably, the LUSC lineage-specific oncogene ΔNp63α serves as a master transcriptional regulator of serine biosynthesis, directly transactivating the expression of PHGDH, PSAT1, PSPH, and SLC1A4. ΔNp63α-driven serine biosynthesis supports nucleotide synthesis and enhances antioxidant defense, enabling cancer cells to survive carboplatin-induced DNA damage and oxidative stress, thereby promoting therapeutic resistance. The combined inhibition of endogenous serine synthesis and restriction of exogenous serine/glycine significantly overcomes ΔNp63α-mediated carboplatin resistance. Our findings establish the ΔNp63α-SSP axis as a critical mechanism driving carboplatin resistance in LUSC. These results highlight dual-targeted disruption of serine availability as a promising therapeutic strategy to overcome chemotherapy resistance in ΔNp63α-driven LUSC. This study underscores the importance of lineage-specific metabolic dependencies as essential targets for precision oncology in NSCLC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.