Nicotine-driven enhancement of tumor malignancy in triple-negative breast cancer via additive regulation of CHRNA9 and IGF1R

J Pathol. 2025 Jun;266(2):230-245. doi: 10.1002/path.6423. Epub 2025 Apr 17.

Abstract

Cigarette smoking is a significant risk factor for cancer development with complex mechanisms. This study aims to investigate the impact of nicotine exposure on the regulation of stemness- and metastasis-related properties via cholinergic receptor nicotinic alpha 9 subunit (CHRNA9) and insulin-like growth factor-1 receptor (IGF1R) and to evaluate their therapeutic potential in triple-negative breast cancer (TNBC). We performed Kaplan-Meier survival analysis of public databases and revealed that high expression of CHRNA9, IGF1R signaling molecules, and stemness genes was significantly associated with poor recurrence-free survival (RFS) and distant metastasis-free survival (DMFS) in TNBC samples. Additionally, we examined two patient cohorts to determine the clinical associations between the expression levels of different genes (n = 67) and proteins (n = 42) and showed a strong positive correlation between the expression levels of CHRNA9, IGF1R signaling molecules, and stemness markers POU5F1/NANOG in tumor tissues. We carried out nicotine treatment and knockdown of CHRNA9 and IGF1R in TNBC cells to identify the effects on stemness-related properties in vitro. Furthermore, primary and secondary metastatic in vivo animal models were examined using micro-computed tomography (μCT) screening and in situ hybridization with a human Alu probe to detect tumor cells. Nicotine was found to upregulate the expression of CHRNA9, POU5F1, and IGF1R, influencing stemness- and metastasis-related properties. Knockdown of CHRNA9 expression attenuated nicotine-induced stemness-related properties in a TNBC cell model. Furthermore, knockdown of IGF1R expression significantly alleviated nicotine/CHRNA9-induced stemness features and cancer cell metastasis in cell cultures and lung metastatic mouse models. These results demonstrate that nicotine triggers IGF1R signaling, thereby enhancing stemness-related properties, cell migration, invasion, and tumor metastasis, resulting in a poorer prognosis for patients with TNBC. These findings highlight IGF1R as a promising therapeutic target for reducing stemness and metastasis in TNBC patients exposed to environmental nicotine. © 2025 The Pathological Society of Great Britain and Ireland.

Keywords: CHRNA9; IGF1R; POU5F1; TNBCs; metastasis; nicotine; recurrence; stemness; survival.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mice
  • Neoplastic Stem Cells* / drug effects
  • Neoplastic Stem Cells* / metabolism
  • Neoplastic Stem Cells* / pathology
  • Nicotine* / toxicity
  • Receptor, IGF Type 1* / genetics
  • Receptor, IGF Type 1* / metabolism
  • Receptors, Nicotinic* / genetics
  • Receptors, Nicotinic* / metabolism
  • Signal Transduction / drug effects
  • Triple Negative Breast Neoplasms* / genetics
  • Triple Negative Breast Neoplasms* / metabolism
  • Triple Negative Breast Neoplasms* / pathology

Substances

  • Nicotine
  • Receptor, IGF Type 1
  • IGF1R protein, human
  • Receptors, Nicotinic
  • CHRNA9 protein, human