ArticleJournal of cancer research and clinical oncology2015
Down-regulation of ALDH1A3, CD44 or MDR1 sensitizes resistant cancer cells to FAK autophosphorylation inhibitor Y15.
Article in Journal of cancer research and clinical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- The pathogenic role of retinoid nuclear receptor signaling in cancer and metabolic syndromes.The Journal of experimental medicine · 2024Review
- circCYP24A1 promotes Docetaxel resistance in prostate Cancer by Upregulating ALDH1A3.Biomarker research · 2022Article
- NAD- and NADPH-Contributing Enzymes as Therapeutic Targets in Cancer: An Overview.Biomolecules · 2020Review
- Structure-Based Optimization of a Novel Class of Aldehyde Dehydrogenase 1A (ALDH1A) Subfamily-Selective Inhibitors as Potential Adjuncts to Ovarian Cancer Chemotherapy.Journal of medicinal chemistry · 2018Article
- Targeting USP22 Suppresses Tumorigenicity and Enhances Cisplatin Sensitivity Through ALDH1A3 Downregulation in Cancer-Initiating Cells from Lung Adenocarcinoma.Molecular cancer research : MCR · 2018Article
- Computational modeling of methionine cycle-based metabolism and DNA methylation and the implications for anti-cancer drug response prediction.Oncotarget · 2018Article
- Aldehyde dehydrogenase activity plays no functional role in stem cell-like properties in anaplastic thyroid cancer cell lines.Endocrine · 2017Article
- Oncogenic targets Mmp7, S100a9, Nppb and Aldh1a3 from transcriptome profiling of FAP and Pirc adenomas are downregulated in response to tumor suppression by Clotam.International journal of cancer · 2017Article
- Targeting cancer stem cell-specific markers and/or associated signaling pathways for overcoming cancer drug resistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy.Nature medicine · 2016Article
- Effects of folylpolyglutamate synthase modulation on global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells.The Journal of nutritional biochemistry · 2016Article
- Cancer Stem Cells in the Thyroid.Frontiers in endocrinology · 2016Review
- Cancer stem cells in human digestive tract malignancies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- The Proportion of ALDEFLUOR-Positive Cancer Stem Cells Changes with Cell Culture Density Due to the Expression of Different ALDH Isoforms.Cancer studies and molecular medicine : open journal · 2015Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
purposeFocal adhesion kinase is an important survival signal in cancer. Recently, we demonstrated that the autophosphorylation inhibitor of FAK, Y15, effectively inhibited cancer cell growth. We detected many cancer cell lines sensitive to Y15 and also detected several cell lines such as colon cancer Lovo-1 and thyroid K1 more resistant to Y15. We sought to determine the main players responsible for the resistance.
methodsTo reveal the signaling pathways responsible for the increased resistance of these cancer cells to the inhibitor of FAK, we performed a microarray gene profile study in both sensitive and resistant cells treated with Y15 inhibitor to compare with the more sensitive cells.
resultsAmong unique genes up-regulated by Y15 in Lovo-1 and K1 resistant cells, a stem cell marker-ALDH1A3-was detected to be up-regulated >twofold. The resistant Lovo-1 and thyroid K1 cells overexpressed ALDH1A3 and CD44 versus sensitive cells. Treatment with ALDH1A3 siRNAs or ALDH inhibitor, DEAB sensitized resistant Lovo-1 and K1 cells to Y15 inhibitor, decreased viability and caused G1 cell cycle arrest more effectively than each agent alone. In addition, down-regulation of CD44 that was overexpressed in resistant Lovo-1 cells with CD44 siRNA effectively decreased the viability of cells in combination with Y15. In addition, down-regulation of overexpressed MDR1 with specific inhibitor, PSC-833, also sensitized resistant colon cancer cells to Y15.
conclusionsThis report clearly demonstrates the mechanism of resistance to FAK autophosphorylation inhibitor and the mechanism to overcome it that is important for developing FAK-targeted therapy approaches.
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