ArticleMolecular medicine (Cambridge, Mass.)2012
Identification of ING4 (inhibitor of growth 4) as a modulator of docetaxel sensitivity in human lung adenocarcinoma.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- MARCKSL1-2 reverses docetaxel-resistance of lung adenocarcinoma cells by recruiting SUZ12 to suppress HDAC1 and elevate miR-200b.Molecular cancer · 2022Article
- An EHMT2/NFYA-ALDH2 signaling axis modulates the RAF pathway to regulate paclitaxel resistance in lung cancer.Molecular cancer · 2022Article
- Multi-Omics Integrative Analysis of Lung Adenocarcinoma: AnFrontiers in medicine · 2022Article
- Mechanisms of resistance to chemotherapy in non-small cell lung cancer.Archives of pharmacal research · 2021Review
- The overexpression of maspin increases the sensitivity of lung adenocarcinoma drug-resistant cells to docetaxelAnnals of translational medicine · 2020Article
- The Biological and Clinical Relevance of Inhibitor of Growth (ING) Genes in Non-Small Cell Lung Cancer.Cancers · 2019Review
- The essential role of tumor suppressor geneBioscience reports · 2019Review
- ING4 suppresses hepatocellular carcinoma via a NF-κB/miR-155/FOXO3a signaling axis.International journal of biological sciences · 2019Article
- Overexpression of Inhibitor of Growth 4 Enhances Radiosensitivity in Non-Small Cell Lung Cancer Cell Line SPC-A1.Technology in cancer research & treatment · 2017Article
- Cancer-associated fibroblasts treated with cisplatin facilitates chemoresistance of lung adenocarcinoma through IL-11/IL-11R/STAT3 signaling pathway.Scientific reports · 2016Article
- Inhibitor of growth-4 is a potential target for cancer therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Tumor suppressor genes and their underlying interactions in paclitaxel resistance in cancer therapy.Cancer cell international · 2016Review
- ING4 enhances paclitaxel's effect on colorectal cancer growth in vitro and in vivo.International journal of clinical and experimental pathology · 2015Article
- Article
- HDAC 1/4-mediated silencing of microRNA-200b promotes chemoresistance in human lung adenocarcinoma cells.Oncotarget · 2014Article
- Secreted frizzled related protein 1 modulates taxane resistance of human lung adenocarcinoma.Molecular medicine (Cambridge, Mass.) · 2014Article
- Prognostic significance of microRNA-141 expression and its tumor suppressor function in human pancreatic ductal adenocarcinoma.Molecular and cellular biochemistry · 2014Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to docetaxel (DTX) usually occurs in patients with lung adenocarcinoma. To better elucidate the underlying molecular mechanisms involved in resistance to DTX-based chemotherapy, we established a DTX-resistant lung adenocarcinoma cell line (SPC-A1/DTX). By gene array analysis, the expression of ING4 was found to be significantly downregulated in SPC-A1/DTX cells. Additionally, the decreased expression of the ING4 gene was induced upon DTX treatment of SPC-A1 cells. Overexpression of ING4 reverses DTX or paclitaxel resistance of DTX-resistant lung adenocarcinoma cells (SPC-A1/DTX or A549/Taxol) by inducing apoptosis enhancement and G₂/M arrest, and small interfering RNA-mediated ING4 knockdown renders DTX-sensitive lung adenocarcinoma cells more resistant to DTX or paclitaxel. Also, overexpression of ING4 could enhance the in vivo sensitivity of SPC-A1/DTX cells to DTX. The phenotypical changes of SPC-A1/DTX cells induced by overexpression of ING4 might be associated with the decreased ratio of Bcl-2/Bax, which resulted in the activation of caspase-3. The level of ING4 expression in tumors of nonresponding patients was significantly lower than that in those of responders, suggesting that the expression of ING4 was positively correlated with tumor response to DTX. Our results provide the first evidence that ING4 might be essential for DTX resistance in lung adenocarcinoma. Thus, ING4 will be a potential molecular target for overcoming resistance to DTX-based chemotherapies in lung adenocarcinoma.
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