ArticleApoptosis : an international journal on programmed cell death2025
ACTG1 mediates cisplatin resistance in NSCLC through induction of mitochondrial fragmentation.
Article in Apoptosis : an international journal on programmed cell death, 2025. 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
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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.
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Who cites it
2 citing papers in PubMed.
- Review
- Do fungi also undergo "ferroptosis"? A microscopic exploration of cellular death.Apoptosis : an international journal on programmed cell death · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Actin gamma 1 (ACTG1) encodes the cytoskeletal protein γ-actin and is overexpressed in various cancers. Cisplatin-based chemotherapy is the standard first-line treatment for patients with advanced non-small cell lung cancer (NSCLC). However, most patients eventually develop cisplatin resistance. The association between ACTG1 and cisplatin resistance remains unclear. In this study, we found that high expression of ACTG1 was associated with poor prognosis in NSCLC. Knockdown of ACTG1 promoted mitochondrial fragmentation via interaction with the fusion protein MFN2 and induced ferroptosis. Mechanistically, ACTG1 knockdown disrupted mitochondrial dynamics, elevated mitochondrial ROS, reduced glutathione (GSH) levels, and enhanced lipid peroxidation. This cascade significantly inhibited the growth of cisplatin-resistant NSCLC cells and sensitized them to cisplatin. Furthermore, the ferroptosis inducer RSL3 synergized with cisplatin to enhance ferroptosis and mitochondrial fragmentation, effectively sensitizing ACTG1-overexpressing cells both in vitro and in xenograft models. Our findings establish ACTG1 as a critical mediator of cisplatin resistance in NSCLC through regulation of mitochondrial integrity and ferroptosis. Targeting the ACTG1-MFN2 axis combined with ferroptosis induction represents a promising therapeutic strategy to overcome cisplatin resistance.
Indexed as
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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.