ArticleMedical oncology (Northwood, London, England)2015
CCR9-CCL25 interaction suppresses apoptosis of lung cancer cells by activating the PI3K/Akt pathway.
Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Soluble cytokines and chemokines in NSCLC: drivers of immune evasion and angiogenesis.Frontiers in immunology · 2026Review
- Preliminary Exploration of Fluvastatin Inhibiting Proliferation, Migration and Invasion of Lung Cancer Cells and Reversing Paclitaxel Resistance: Mechanism Exploration Based on Multi-Omics Analysis.Drug design, development and therapy · 2026Article
- Enhanced inhibitory effects of mianserin in combination with sorafenib on liver cancer growth through targeting the CCR9-AKT pathway.American journal of cancer research · 2025Article
- The novel functions of chemokines in lung cancer progression.Frontiers in immunology · 2025Review
- Genetic variants ofFrontiers in immunology · 2024Article
- Determination of the Binding Epitope of an Anti-Mouse CCR9 Monoclonal Antibody (CAntibodies (Basel, Switzerland) · 2023Article
- Characteristics and Resistance to Cisplatin of Human Neuroblastoma Cells Co-Cultivated with Immune and Stromal Cells.Bioengineering (Basel, Switzerland) · 2022Article
- Therapeutic potential of an anti-CCR9 mAb evidenced in xenografts of human CCR9Frontiers in immunology · 2022Article
- Advances in Research on the Effects and Mechanisms of Chemokines and Their Receptors in Cancer.Frontiers in pharmacology · 2022Review
- CCL25/CCR9 interaction promotes the malignant behavior of salivary adenoid cystic carcinomaPeerJ · 2022Article
- TIPE polarity proteins are required for mucosal deployment of T lymphocytes and mucosal defense against bacterial infection.Molecular biomedicine · 2021Article
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- Identification of hub genes in gastric cancer by integrated bioinformatics analysis.Translational cancer research · 2021Article
- [Synergistic effect of polysaccharide fromNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Article
- 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
- CCL25 promotes the migration and invasion of non-small cell lung cancer cells by regulating VEGF and MMPs in a CCR9-dependent manner.Experimental and therapeutic medicine · 2020Article
- The CC and CXC chemokines: major regulators of tumor progression and the tumor microenvironment.American journal of physiology. Cell physiology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CC chemokine receptor-9 (CCR9) is highly expressed in non-small cell lung cancer (NSCLC) tissues and cell lines. However, the biological functions and the signals elicited by the interaction between CCR9 and its natural ligand CCL25 in NSCLC are unknown. Here, we selectively depleted CCR9 and inhibited CCR9-CCL25 interaction in NSCLC cells using small recombinant lentivirus-mediated miRNA, and investigated the tumorigenic effects in vitro and in vivo. Compromised CCR9-CCL25 interaction promoted apoptosis in NSCLC cells by activating phosphoinositide 3-kinase (PI3K)/Akt in vitro. In addition, we showed that CCR9-CCL25 interaction mediated the activation of the PI3K/Akt pathway in NSCLC cells, resulting in the up-regulation of anti-apoptotic proteins, as well as the down-regulation of apoptotic proteins in a PI3K-/Akt-dependent manner. These CCR9-CCL25-mediated effects were abrogated in the presence of a PI3K inhibitor (wortmannin 10 nM) or by inhibiting the CCR9-CCL25 interaction through CCR9 silencing, which also suggested that the biological function of CCR9-CCL25 was mainly regulated by PI3K. In vivo studies also demonstrated a significantly lower tumor burden in mice receiving CCR9-silence cells than those in mice receiving control cells. Together, these data suggested that CCR9-CCL25 interaction induced tumorigenesis of NSCLC cells and that this induction might be accomplished through the activation of the PI3K/Akt pathway. These findings may lead to a better understanding of the biological effects of CCR9-CCL25 interaction and provide clues for identifying novel therapeutic and preventive molecular markers for NSCLC.
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Registered trials
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.