ArticleOncology letters2019
Placenta-specific 8 is a potential novel target for osimertinib resistance in non-small cell lung cancer.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- ALDH1: A potential therapeutic target for cancer stem cells in solid tumors.Frontiers in oncology · 2022Review
- Multifaced roles of PLAC8 in cancer.Biomarker research · 2021Review
- Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer.Communications biology · 2021Article
- Whole-transcriptome Analysis of Fully Viable Energy Efficient Glycolytic-null Cancer Cells Established by Double Genetic Knockout of Lactate Dehydrogenase A/B or Glucose-6-Phosphate Isomerase.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Currently, osimertinib (AZD9291) is the only third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor approved by the Food and Drug Administration for the treatment of non-small cell lung cancer (NSCLC) with EGFR T790M mutations. However, acquired resistance is an inevitable clinical challenge. Although placenta-specific 8 (PLAC8) has been proven to serve an important role in tumor progression and resistance, its effect in AZD9291 resistance in NSCLC remains largely unknown. The aim of the present study was to investigate the functional role of PLAC8 in AZD9291 resistance in NSCLC. The results revealed that the level of PLAC8 was significantly upregulated in AZD9291-resistant cells compared with that in parent cells. Overexpression of PLAC8 in parent cells markedly decreased drug sensitivity, and enhanced cell proliferation, colony formation and migration. Furthermore, the levels of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were observed to be upregulated in resistant cells and PLAC8-overexpressing parent cells, suggesting that ALDH1A1 may be involved in the association between the overexpression of PLAC8 and AZD9291 resistance in NSCLC. Overall, PLAC8 overexpression promoted NSCLC resistance to AZD9291, and PLAC8 may be a potential target for the reversal of AZD9291 resistance.
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