ArticleThoracic cancer2016
Small activating ribonucleic acid reverses tyrosine kinase inhibitor resistance in epidermal growth factor receptor-mutant lung cancer by increasing the expression of phosphatase and tensin homolog.
Article in Thoracic cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Small Activating RNAs: A Curated Database and an Overview of Rational Design Principles.Molecules (Basel, Switzerland) · 2026Review
- Biomimetic proteolipid vesicles delivering small activating RNA to activate the macrophage immunotherapy for the treatment of lung cancer.Journal of nanobiotechnology · 2026Article
- Non-Viral RNA Therapies for Non-Small Cell Lung Cancer and Their Corresponding Clinical Trials.Molecular pharmaceutics · 2025Review
- Modulating the expression of tumor suppressor genes using activating oligonucleotide technologies as a therapeutic approach in cancer.Molecular therapy. Nucleic acids · 2023Review
- Emerging Progress of RNA-Based Antitumor Therapeutics.International journal of biological sciences · 2023Review
- The biochemical and clinical implications of phosphatase and tensin homolog deleted on chromosome ten in different cancers.American journal of cancer research · 2021Review
- [Mechanisms of Resistance to the Third-generation Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018Review
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
backgroundEpidermal growth factor receptor-tyrosine kinase inhibitors (TKI-EGFRs) present a new prospect for the treatment of lung cancer. However, in clinical application, the majority of patients become TKI resistant within a year. More and more studies have shown that a loss of phosphatase and tensin homolog (PTEN) expression is associated with TKI resistance. An alternative method of upregulating PTEN expression may reverse TKI resistance.
methodsWe designed five candidate small activating ribonucleic acids (saRNAs) to target PTEN, and transfected them into H-157 cells to screen out functional saRNA. We used reverse transcriptase-polymerase chain reaction and Western blot to evaluate the effect of saRNA to PTEN expression. We then analyzed the growth and apoptosis of cells transfected with saRNA under the treatment of TKI to investigate whether saRNAs can reverse TKI resistance by upregulating PTEN expression.
resultsThe functional saRNA we designed could upregulate PTEN expression. The H-157 cells transfected with saRNA grew slower in the presence of TKI drugs than the cells that were not transfected with saRNA. The apoptosis rate was also obviously higher.
conclusionsOur study proves that loss of PTEN expression is an important mechanism of TKI resistance. It is possible to control TKI resistance by upregulating PTEN expression using RNA activation technology.
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