ArticleCancer genomics & proteomics
Paclitaxel Impedes EGFR-mutated PC9 Cell Growth
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Mechanism-based management of taxane-induced neuropathic pain in breast cancer survivors: a critical review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Paclitaxel-induced germline DNA-damage signatures independent of mismatch repair inFrontiers in pharmacology · 2026Article
- Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025Review
- Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024Review
- Pan-EGFR Inhibitor Dacomitinib Resensitizes Paclitaxel and Induces Apoptosis via Elevating Intracellular ROS Levels in Ovarian Cancer SKOV3-TR Cells.Molecules (Basel, Switzerland) · 2024Article
- Exploring the Potential of Lapatinib, Fulvestrant, and Paclitaxel Conjugated with Glycidylated PAMAM G4 Dendrimers for Cancer and Parasite Treatment.Molecules (Basel, Switzerland) · 2023Article
- Asparagus officinalis combined with paclitaxel exhibited synergistic anti-tumor activity in paclitaxel-sensitive and -resistant ovarian cancer cells.Journal of cancer research and clinical oncology · 2023Article
- Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2023Review
- Toward the next generation EGFR inhibitors: an overview of osimertinib resistance mediated by EGFR mutations in non-small cell lung cancer.Cell communication and signaling : CCS · 2023Review
- The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products.Antioxidants (Basel, Switzerland) · 2022Review
- Metformin Attenuates UVA-Induced Skin Photoaging by Suppressing Mitophagy and the PI3K/AKT/mTOR Pathway.International journal of molecular sciences · 2022Article
- Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimPaclitaxel is used as a first-line and subsequent therapy for the treatment of various cancers. However, the function and mechanisms of action of paclitaxel in non-small-cell lung cancer (NSCLC) remain unknown. In this study, the molecular mechanism underlying the anticancer activity of paclitaxel was investigated in vitro in a human NSCLC cell line carrying the EGFR exon 19 deletion (PC9). MATERIALS AND
methodsPC9 cells were treated with paclitaxel and then evaluated with a cell viability assay, DAPI staining, Giemsa staining, apoptosis assay, reactive oxygen species (ROS) assay, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and Western blotting.
resultsPaclitaxel markedly decreased the viability of PC9 cells and induced morphological signs of apoptosis. The apoptotic effects of paclitaxel were observed through caspase cascade activation, along with ROS generation and loss of mitochondrial membrane potential (MMP). Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation. In addition, we found that paclitaxel effectively suppressed the EGFR/PI3K/AKT/mTOR signaling pathway to impede PC9 cell growth. Paclitaxel induced cell cycle arrest at the G1 phase in response to DNA damage, in association with the suppression of CDC25A, Cdk2 and Cyclin E1 protein expression.
conclusionPaclitaxel showed anticancer effects against NSCLC by activating extrinsic and intrinsic apoptotic pathways through enhancing ROS generation, inducing cell cycle arrest, and suppressing EGFR/PI3K/AKT/mTOR signaling 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.