ArticleContemporary oncology (Poznan, Poland)2013
Research on drug resistance mechanism of trastuzumab caused by activation of the PI3K/Akt signaling pathway.
Article in Contemporary oncology (Poznan, Poland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Mechanism of trastuzumab resistance caused by HER-2 mutation in breast carcinomas.Cancer management and research · 2019Article
- Application of the CRISPR/Cas9 System to Drug Resistance in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2018Review
- The effect of tetrandrine combined with cisplatin on proliferation and apoptosis of A549/DDP cells and A549 cells.Cancer cell international · 2017Article
- The chemomodulatory effects of resveratrol and didox on herceptin cytotoxicity in breast cancer cell lines.Scientific reports · 2015Article
- Deguelin induces the apoptosis of lung cancer cells through regulating a ROS driven Akt pathway.Cancer cell international · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aim of the studyTo discuss the activation of the signal transduction pathway of phosphatidylinositol 3'-kinase/serine-threonine kinase (PI3K/Akt), one of the important targets of drug resistance of trastuzumab, which provides a theoretical basis for the targeted therapy of drug resistance of trastuzumab in breast cancer. MATERIAL AND
methodsEstablish the drug-resistance sub-strain BT-HerR of trastuzumab for the continuous treatment of human breast cancer cell strain BT474, conduct Her-2 phenotype analysis on the drug-resistance cell strain BT-HerR with the FISH method, detect the proliferation inhibition in vitro of trastuzumab to BT474 and BT-HerR cells with the MTT method, detect the apoptosis variation after interference of trastuzumab with a flow cytometer and detect p-Akt and apoptosis-related protein expression with Western blot after PI3K/Akt inhibitor LY294002 interferes with the cells.
resultsThe gene expression of drug-resistance cell strain BT-HerR Her-2 is strongly positive; 72 hours after interference of trastuzumab, the proliferation in vitro of the BT474 and BT-HerR cells is inhibited, which is strengthened with the increase of concentration, showing a significant difference (p < 0.01); after treatment of trastuzumab, comparison of the cell apoptosis rate of BT474 and BT-HerR shows a significant difference (p < 0.01); trastuzumab can only inhibit the Akt protein phosphorylation of BT474, while LY294002 can inhibit the BT-HerR and BT474 Akt protein phosphorylation simultaneously.
conclusionsAkt protein phosphorylation of trastuzumab drug-resistance cells is activated; LY294002, a PI3K/Akt inhibitor, can obviously inhibit Akt protein phosphorylation of trastuzumab drug-resistance cells and there is a clear association between the PI3K/Akt signal transduction pathway and trastuzumab resistance.
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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.