ArticleCancer biology & therapy2015
Activation of IL-8 via PI3K/Akt-dependent pathway is involved in leptin-mediated epithelial-mesenchymal transition in human breast cancer cells.
Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Association Between Leptin (-2548G/A) Genes Polymorphism and Breast Cancer Susceptibility: A Meta-Analysis.Medicine · 2016Pooled it
- Remodeling the Immune Landscape: How Obesity-Induced SASPs Create a Pro-Tumorigenic Niche.Current obesity reports · 2026Review
- Leptin Signaling at the Crossroads of Obesity, Immunity, and Cancer: Mechanistic Insights and Therapeutic Implications.Biomolecules & therapeutics · 2026Review
- IL-8 drives EMT and malignant progression in chronic obstructive pulmonary disease-associated lung cancer via STAT3 signaling.Cell division · 2026Article
- Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review).International journal of oncology · 2026Review
- Oncotransformation in Bhas 42 Cell Transformation Assay by Typical Non-Genotoxic Carcinogens, PFOA and PFOS, and Time-Course Transcriptome Analysis.Biomolecules · 2025Article
- Immunoregulatory mechanisms in the aging microenvironment: Targeting the senescence-associated secretory phenotype for cancer immunotherapy.Acta pharmaceutica Sinica. B · 2025Review
- The role of HOXA1 in cancer and targeted therapy.Medical oncology (Northwood, London, England) · 2025Review
- The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Regulation of Cellular Senescence in Cancer.Biomolecules · 2025Review
- The crosstalk between senescence, tumor, and immunity: molecular mechanism and therapeutic opportunities.MedComm · 2025Review
- Senescent immune cells in the tumor microenvironment: emerging insights into cancer immunotherapy resistance.Frontiers in immunology · 2025Review
- Leptin secreted by adipocytes promotes EMT transition and endometrial cancer progression via the JAK2/STAT3 signalling pathway.Adipocyte · 2024Article
- A preliminary mechanistic exploration of the effect of leptin on the docetaxel sensitivity of MDA‑MB‑231 triple‑negative breast cancer cells.Molecular and clinical oncology · 2024Article
- Article
- Autophagy induced by Helicobacter Pylori infection can lead to gastric cancer dormancy, metastasis, and recurrence: new insights.Human cell · 2024Review
- Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.Frontiers in allergy · 2024Review
- Contents of exosomes derived from adipose tissue and their regulation on inflammation, tumors, and diabetes.Frontiers in endocrinology · 2024Review
- 3D bioprinted breast tumor-stroma models for pre-clinical drug testing.Materials today. Bio · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background informationPrevious studies have revealed that leptin may be involved in epithelial-mesenchymal transition (EMT), a crucial initiator of cancer progression to facilitate metastatic cascade, increase tumor recurrence, and ultimately cause poor prognosis. However, the underlying mechanism remains unclear. The aim of our present study was to investigate the effect of leptin on EMT of breast cancer cells and the underlying mechanism.
resultsOur data demonstrated that leptin significantly increased the phosphorylation of STAT3, Akt, and ERK1/2, elevated the expression of IL-8, and induced breast cancer cells to undergo EMT. The effect of leptin on IL-8 could visibly abolished by the inhibitor of PI3K LY294002. In addition, leptin-induced EMT of breast cancer cells was blocked by anti-IL-8 antibodies. Examination of the expression of ObR, leptin, IL-8 and EMT-related biomarkers in patient specimens demonstrated that malignant breast carcinoma with lymph node metastases (LNM), which represents poor prognosis, expressed higher levels of ObR, leptin, IL-8 than other types of breast cancer, and displayed more obvious EMT transversion. In vivo xenograft experiment revealed that leptin signally promoted tumor growth and metastasis and increased the expressions of IL-8 and EMT-related biomarkers.
conclusionsOur results support that leptin-induced EMT in breast cancer cells requires IL-8 activation via the PI3K/Akt signal pathway.
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