ArticleNeoplasia (New York, N.Y.)2012
Long-term smoking mediated down-regulation of Smad3 induces resistance to carboplatin in non-small cell lung cancer.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Identification of stage-specific biomarkers in lung adenocarcinoma based on RNA-seq data.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- DNA methylation profiles of bronchoscopic biopsies for the diagnosis of lung cancer.Clinical epigenetics · 2021Article
- Smoking status and pathological response to neoadjuvant chemotherapy among patients with bladder cancer: a pooled analysis.Translational andrology and urology · 2021Article
- MiR-216b/Smad3/BCL-2 Axis Is Involved in Smoking-Mediated Drug Resistance in Non-Small Cell Lung Cancer.Cancers · 2020Article
- Cathepsin L-mediated resistance of paclitaxel and cisplatin is mediated by distinct regulatory mechanisms.Journal of experimental & clinical cancer research : CR · 2019Article
- Paclitaxel increases the sensitivity of lung cancer cells to lobaplatin via PI3K/Akt pathway.Oncology letters · 2018Article
- Targeting focal adhesion kinase overcomes erlotinib resistance in smoke induced lung cancer by altering phosphorylation of epidermal growth factor receptor.Oncoscience · 2018Article
- Article
- Chronic exposure to cigarette smoke leads to activation of p21 (RAC1)-activated kinase 6 (PAK6) in non-small cell lung cancer cells.Oncotarget · 2016Article
- The Emerging Role of Extracellular Vesicle-Mediated Drug Resistance in Cancers: Implications in Advanced Prostate Cancer.BioMed research international · 2015Review
- Encapsulation in nanoparticles improves anti-cancer efficacy of carboplatin.AAPS PharmSciTech · 2014Article
- A genome-wide gene-environment interaction analysis for tobacco smoke and lung cancer susceptibility.Carcinogenesis · 2014Article
- Nicotine-mediated cell proliferation and tumor progression in smoking-related cancers.Molecular cancer research : MCR · 2014Review
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
While numerous cell signaling pathways are known to play decisive roles in chemotherapeutic response, relatively little is known about the impact of the Smad-dependent transforming growth factor β pathway on the therapeutic outcome. Previous reports suggested that patients with lung cancer who continue to smoke while receiving chemotherapy have a poorer outcome than their nonsmoking counterparts do. In our previous study, we showed that long-term cigarette smoke condensate (CSC)-mediated down-regulation of Smad3 induces tumorigenesis. The objective of this study was to determine the mechanism of function of Smad3 in chemoresistance induced by CSC in human lung cell lines, namely, A549 and HPL1A. Long-term CSC treatment increases the half-maximal inhibitory concentration (IC(50)) of carboplatin and makes cells resistant to carboplatin. The increase in IC(50) of long-term CSC-treated cells is due to the reduced induction in apoptosis by carboplatin. The increase in IC(50) and decrease in apoptosis in long-term CSC-treated cells is correlated with the expression of Bcl2. We have determined that Bcl2 is both necessary and sufficient to make the cells resistant to carboplatin. We have also shown that Smad3 acts upstream to regulate the expression of Bcl2 specifically and, thus, sensitivity of the cells to carboplatin. This is supported by the inverse correlation between the expressions of Smad3 and Bcl2 in human lung tumors. Collectively, these data suggest that loss of Smad3 expression in CSC-treated cells induces resistance to carboplatin by upregulating the expression of Bcl2. This study explains, at least in part, the higher chemoresistance rate observed in smokers.
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