ArticleBreast cancer research and treatment2014
Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3.
Article in Breast cancer research and treatment, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Targeting Modifiable Risks: Molecular Mechanisms and Population Burden of Lifestyle Factors on Male Genitourinary Health.International journal of molecular sciences · 2025Pooled it
- Neurotransmitters: an emerging target for therapeutic resistance to tumor immune checkpoint inhibitors.Molecular cancer · 2025Review
- α9 Nicotinic Acetylcholine Receptor Promotes Tumor Proliferation and Suppresses Ferroptosis in Triple-Negative Breast Cancer.Biomolecules · 2025Article
- A dataset of chronic nicotine-induced genes in breast cancer cells.Data in brief · 2025Article
- Galectin-3 in Cardiovascular Health: A Narrative Review Based on Life's Essential 8 and Life's Simple 7 Frameworks.Current issues in molecular biology · 2025Review
- S100A8/A9 innate immune signaling as a distinct mechanism driving progression of smoking-related breast cancers.Oncogene · 2025Article
- The angiogenic role of the alpha 9-nicotinic acetylcholine receptor in triple-negative breast cancers.Angiogenesis · 2024Article
- The angiogenic role of the alpha 9-nicotinic acetylcholine receptor in triple-negative breast cancers.Angiogenesis · 2024Article
- N-Glycosylation Deficiency in Transgene α7 nAChR and RIC3 Expressing CHO Cells Without NACHO.The Journal of membrane biology · 2024Article
- Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- CHRNA9 as a New Prognostic Marker and Potential Therapeutic Target in Glioma.Journal of Cancer · 2024Article
- Development of Galectin-3 Targeting Drugs for Therapeutic Applications in Various Diseases.International journal of molecular sciences · 2023Review
- Nicotinic acetylcholine receptors: Therapeutic targets for novel ligands to treat pain and inflammation.Pharmacological research · 2023Review
- Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview.International journal of molecular sciences · 2023Article
- Exploring neurotransmitters and their receptors for breast cancer prevention and treatment.Theranostics · 2023Review
- Smoking Cessation after Cancer Diagnosis and Enhanced Therapy Response: Mechanisms and Significance.Current oncology (Toronto, Ont.) · 2022Review
- The potential role of nicotine in breast cancer initiation, development, angiogenesis, invasion, metastasis, and resistance to therapy.Breast cancer (Tokyo, Japan) · 2022Review
- Nicotine-induced miR-21-3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a.Oncology letters · 2022Article
- α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells.Marine drugs · 2021Article
- Multi-Omics Analysis of the Effects of Smoking on Human Tumors.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nicotine, a main addictive compound in tobacco smoke, has been linked to promotion and progression of lung, head and neck, pancreatic, and breast cancers, but the detailed mechanisms of cancer progression remain elusive. Here, we show that nicotine induces the expression of galectin-3 (an anti-apoptotic β-galactoside-binding lectin) in breast cancer cell line and in primary tumors from breast cancer patients. Nicotine-induced up regulation of galectin-3 is due to an increased expression of α9 isoform of nicotinic acetylcholine receptor (α9nAChR), which activates transcription factor STAT3 that in turn, physically binds to galectin-3 (LGALS3) promoter and induces transcription of galectin-3. Intracellular galectin-3 increased mitochondrial integrity and suppressed chemotherapeutic-induced apoptosis of breast cancer cell. Moreover, nicotine-induced enrichment of side population cells with cancer stem cell-like properties was modulated by galectin-3 expression and could be significantly reduced by transient knock down of LGALS3 and its upstream signaling molecules STAT3 and α9nAChR. Thus, galectin-3 or its upstream signaling molecule STAT3 or α9nAChR could be a potential target to prevent nicotine-induced chemoresistance in breast cancer.
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Registered trials
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