ArticleDrug design, development and therapy2021
RASSF1A Enhances Chemosensitivity of NSCLC Cells Through Activating Autophagy by Regulating MAP1S to Inactivate Keap1-Nrf2 Pathway.
Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- A mechanistic study revealing that SLCO1B3 promotes gastric cancer development and metastasis through MAP1S expression downregulation.BMC cancer · 2026Article
- Multi-omics integration in deciphering non-small cell lung cancer drug resistance: current status, challenges, and future prospects.Hereditas · 2026Review
- Baicalin promotes the sensitivity of NSCLC to cisplatin by regulating ferritinophagy and macrophage immunity through the KEAP1-NRF2/HO-1 pathway.European journal of medical research · 2024Article
- [Research Progress of DNA Methylation in Cisplatin Resistance in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Review
- Is Autophagy Always a Barrier to Cisplatin Therapy?Biomolecules · 2022Review
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCisplatin (DDP) is an effective first-line therapy for non-small cell lung cancer (NSCLC) treatment; however, it can cause resistance and thus pose an obstacle to the efficacy of chemotherapy in NSCLC. This study aims to detect the effect of RASSF1A on DDP resistance of NSCLC and the underlying mechanism.
methodsThe expression levels of RASSF1A and microtubule-associated protein 1S (MAP1S) were investigated by qRT-PCR and Western blot and their interaction was testified by co-immunoprecipitation (Co-IP) analysis. The IC
resultsRASSF1A and MAP1S were lowly expressed and positively correlated in NSCLC tissues. We observed that RASSF1A and MAP1S overexpression significantly enhanced DDP-induced effects in A549 and A549/DDP cells, including decreased cell viability, as well as increased autophagy levels. Besides, investigations into the mechanism between RASSF1A and MAP1S disclosed that RASSF1A could regulate MAP1S to inactivate the Keap1-Nrf2 pathway, thus activating autophagy to enhance chemosensitivity. Moreover, consistent results were confirmed in vivo experiments.
conclusionRASSF1A increases chemosensitivity in NSCLC by facilitating autophagy via MAP1S-mediated Keap1-Nrf2 pathway.
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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.