ArticleWorld journal of surgical oncology2011
CCR9-CCL25 interactions promote cisplatin resistance in breast cancer cell through Akt activation in a PI3K-dependent and FAK-independent fashion.
Article in World journal of surgical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Advances in intratumoral immunotherapy from a neuro-immune-endocrine perspective for breast cancer treatment.Frontiers in oncology · 2026Review
- Differential effect of targeting cisplatin-induced nitrative stress using MnTBAP in auditory and cancer cells.Current research in toxicology · 2025Article
- E2F-1-Akt1 Interaction as Precursor to Cisplatin-induced Apoptosis in Triple-negative Breast Cancer Cells.Oman medical journal · 2025Article
- DNA methylation molecular subtypes for prognosis prediction in lung adenocarcinoma.BMC pulmonary medicine · 2022Article
- Single-Cell Transcriptome Analysis Reveals Changes of Tumor Immune Microenvironment in Oral Squamous Cell Carcinoma After Chemotherapy.Frontiers in cell and developmental biology · 2022Article
- CCR9 initiates epithelial-mesenchymal transition by activating Wnt/β-catenin pathways to promote osteosarcoma metastasis.Cancer cell international · 2021Article
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- CCL25 and CCR9 is a unique pathway that potentiates pannus formation by remodeling RA macrophages into mature osteoclasts.European journal of immunology · 2021Article
- CCL25 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands.International journal of molecular sciences · 2020Review
- Chemokines and chemokine receptors: A new strategy for breast cancer therapy.Cancer medicine · 2020Review
- Role of CC Chemokines Subfamily in the Platinum Drugs Resistance Promotion in Cancer.Frontiers in immunology · 2020Review
- lncRNA MALAT1 Promotes EMT Process and Cisplatin Resistance of Oral Squamous Cell Carcinoma via PI3K/AKT/m-TOR Signal Pathway.OncoTargets and therapy · 2020Article
- CC chemokines are differentially expressed in Breast Cancer and are associated with disparity in overall survival.Scientific reports · 2019Article
- 4T1 Mammary Carcinoma Colonization of Metastatic Niches Is Accelerated by Obesity.Frontiers in oncology · 2019Article
- The role of chemokine receptor 9/chemokine ligand 25 signaling: From immune cells to cancer cells.Oncology letters · 2018Review
- C-C Motif Chemokine Receptor 9 Exacerbates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction.Journal of the American Heart Association · 2016Article
- Chemokine receptor patterns in lymphocytes mirror metastatic spreading in melanoma.The Journal of clinical investigation · 2016Article
- CCR9 in cancer: oncogenic role and therapeutic targeting.Journal of hematology & oncology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChemotherapy heavily relies on apoptosis to kill breast cancer (BrCa) cells. Many breast tumors respond to chemotherapy, but cells that survive this initial response gain resistance to subsequent treatments. This leads to aggressive cell variants with an enhanced ability to migrate, invade and survive at secondary sites. Metastasis and chemoresistance are responsible for most cancer-related deaths; hence, therapies designed to minimize both are greatly needed. We have recently shown that CCR9-CCL25 interactions promote BrCa cell migration and invasion, while others have shown that this axis play important role in T cell survival. In this study we have shown potential role of CCR9-CCL25 axis in breast cancer cell survival and therapeutic efficacy of cisplatin.
methodsBromodeoxyuridine (BrdU) incorporation, Vybrant apoptosis and TUNEL assays were performed to ascertain the role of CCR9-CCL25 axis in cisplatin-induced apoptosis of BrCa cells. Fast Activated Cell-based ELISA (FACE) assay was used to quantify In situ activation of PI3Kp85, AktSer473, GSK-3βSer9 and FKHRThr24 in breast cancer cells with or without cisplatin treatment in presence or absence of CCL25.
resultsCCR9-CCL25 axis provides survival advantage to BrCa cells and inhibits cisplatin-induced apoptosis in a PI3K-dependent and focal adhesion kinase (FAK)-independent fashion. Furthermore, CCR9-CCL25 axis activates cell-survival signals through Akt and subsequent glycogen synthase kinase-3 beta (GSK-3β) and forkhead in human rhabdomyosarcoma (FKHR) inactivation. These results show that CCR9-CCL25 axis play important role in BrCa cell survival and low chemotherapeutic efficacy of cisplatin primarily through PI3K/Akt dependent fashion.
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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.