ArticleJournal of immunology research2019
Mutated p53 Promotes the Symmetric Self-Renewal of Cisplatin-Resistant Lung Cancer Stem-Like Cells and Inhibits the Recruitment of Macrophages.
Article in Journal of immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- Tissue mechanics in tumor heterogeneity and aggression.Trends in cancer · 2025Review
- Activating p53 abolishes self-renewal of quiescent leukaemic stem cells in residual CML disease.Nature communications · 2024Article
- [Lung Cancer Stem-like Cells and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Triple-negative expression (ALDH1A1-/CD133-/mutant p53-) cases in lung adenocarcinoma had a good prognosis.Scientific reports · 2022Article
- Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer.Scientific reports · 2021Article
- Low-dose Diosbulbin-B (DB) activates tumor-intrinsic PD-L1/NLRP3 signaling pathway mediated pyroptotic cell death to increase cisplatin-sensitivity in gastric cancer (GC).Cell & bioscience · 2021Article
- Cancer Stemness Meets Immunity: From Mechanism to Therapy.Cell reports · 2021Review
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
It has been proposed that mutant p53 is correlated with the recurrence of lung cancer. Recently, a small population of cells with asymmetric or symmetric self-renewal potential has been identified in lung cancer, which was termed as cancer stem-like cells (CSCs) and was speculated to be the reason for cancer recurrence after chemotherapy. In this study, we used lung cancer cell lines with different TP53 backgrounds to elucidate the potential role of mutant p53 in regulating lung CSC self-renewal and on lung cancer recurrence. Cisplatin-resistant lung cancer cells with different TP53 backgrounds were generated
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