ArticleCancer gene therapy2026
From resistance to sensitivity: the impact of FADD and lncRNA PPFIA1-AS1 on cisplatin treatment in LUSC.
Article in Cancer gene therapy, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin resistance remains a significant challenge in treating lung squamous cell carcinoma (LUSC). The role of FADD in this resistance requires further investigation. Our study revealed that FADD is overexpressed in LUSC patients, correlating with lower survival rates. We also discovered that long-term cisplatin-resistant LUSC cell lines (LUSC-CR) had elevated FADD protein levels, and reducing FADD restored their cisplatin sensitivity. At the same time, LUSC-CR cells resisted cisplatin-induced DNA damage and had enhanced DNA repair, linked to P53's negative regulation of FADD. Additionally, knockdown of the long non-coding RNA (lncRNA) PPFIA1-AS1 can potentiate drug resistance in LUSC cells by decelerating FADD protein turnover and elevating FADD protein levels. In essence, this study elucidated novel mechanisms underlying cisplatin resistance in LUSC, wherein the PPFIA1-AS1/FADD axis regulates DNA damage and repair. Consequently, targeting the PPFIA1-AS1/FADD axis may present a promising avenue for overcoming cisplatin resistance and enhancing the prognosis of LUSC patients.
Indexed as
Identifiers
41238771What 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.