ArticleOncology reports2019
let‑7 and miR‑17 promote self‑renewal and drive gefitinib resistance in non‑small cell lung cancer.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- miR-17: from developmental regulatory hub to molecular engine driving tumourigenesis.Frontiers in oncology · 2026Review
- Targeting Oncogenic miRNAs in NSCLC: Therapeutic Strategies and Emerging Approaches.Cancer management and research · 2026Review
- The Role and Therapeutic Potential of Non-coding RNAs in Resistance to EGFR - TKIs Targeted Therapy for Non-small Cell Lung Cancer.Current medicinal chemistry · 2025Review
- Comprehensive review of LncRNA-mediated therapeutic resistance in non-small cell lung cancer.Cancer cell international · 2024Review
- Let-7a-3p overexpression increases chemosensitivity to carmustine and synergistically promotes autophagy and suppresses cell survival in U87MG glioblastoma cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- Recent advances on high-efficiency of microRNAs in different types of lung cancer: a comprehensive review.Cancer cell international · 2023Review
- Composition of Conditioned Media from Radioresistant and Chemoresistant Cancer Cells Reveals miRNA and Other Secretory Factors Implicated in the Development of Resistance.International journal of molecular sciences · 2023Review
- Regulation of the Cell Cycle by ncRNAs Affects the Efficiency of CDK4/6 Inhibition.International journal of molecular sciences · 2023Review
- The Small RNA Landscape in NSCLC: Current Therapeutic Applications and Progresses.International journal of molecular sciences · 2023Review
- MicroRNAs and Drug Resistance in Non-Small Cell Lung Cancer: Where Are We Now and Where Are We Going.Cancers · 2022Review
- MiRNAs in Lung Cancer: Diagnostic, Prognostic, and Therapeutic Potential.Diagnostics (Basel, Switzerland) · 2022Review
- MYC Promotes Tyrosine Kinase Inhibitor Resistance in ROS1-Fusion-Positive Lung Cancer.Molecular cancer research : MCR · 2022Article
- Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022Review
- MIR17HG polymorphisms contribute to high-altitude pulmonary edema susceptibility in the Chinese population.Scientific reports · 2022Article
- Cell Behavior of Non-Small Cell Lung Cancer Is at EGFR and MicroRNAs Hands.International journal of molecular sciences · 2021Review
- MicroRNA expression profiling and biomarker validation in treatment-naïve and drug resistant non-small cell lung cancer.Translational lung cancer research · 2021Article
- Advances of exosome isolation techniques in lung cancer.Molecular biology reports · 2020Review
- Triptolide inhibits epithelial‑mesenchymal transition and induces apoptosis in gefitinib‑resistant lung cancer cells.Oncology reports · 2020Article
- Alterations of cell cycle genes in cancer: unmasking the role of cancer stem cells.Molecular biology reports · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor‑tyrosinase kinase inhibitor (EGFR‑TKI) resistance represents a major obstacle in the therapy of non‑small cell lung cancer (NSCLC), and the underlying molecular mechanisms are unknown. In this study, it was found that let‑7 family expression was downregulated and miR‑17 family expression was upregulated in gefitinib‑resistant PC9/GR cells compared with gefitinib‑sensitive PC9 cells. The downregulation of let‑7 and upregulation of miR‑17 have significant clinical relevance to gefitinib resistance in NSCLC. Moreover, it was shown that downregulation of let‑7 and upregulation of miR‑17 promoted resistance to gefitinib by regulating the self‑renewal capability of NSCLC cells. In addition, let‑7 participated in the maintenance of stem cell characteristics by regulating the target gene MYC, and miR‑17 participated in regulation of the cell cycle by regulating the target gene CDKN1A. In NSCLC cells, low expression of let‑7 increased MYC expression to help maintain the undifferentiated status, and high expression of miR‑17 decreased CDKN1A expression to help maintain the proliferative potential. Thus, both let‑7 and miR‑17 promoted self‑renewal, which is typical of stem cell‑like characteristics and resulted in gefitinib resistance. Therefore, this study demonstrated that let‑7 and miR‑17 were involved in the regulation of EGFR‑TKI resistance, and could be used as predictive biomarkers of EGFR‑TKI resistance in NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
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.