2. Academic Validation
  3. GCF2 mediates nicotine-induced cancer stemness and progression in hepatocellular carcinoma

GCF2 mediates nicotine-induced cancer stemness and progression in hepatocellular carcinoma

  • Ecotoxicol Environ Saf. 2024 Jan 11:271:115952. doi: 10.1016/j.ecoenv.2024.115952.
Jinping Li 1,  Dayun Tuo 2,  Tan Cheng 3,  Zhenyan Deng 4,  Jinfeng Gan 5
Affiliations

Affiliations

  • 1 Department of Histology and Embryology, School of Preclinical Medicine, Guilin Medical University, Guilin, Guangxi, PR China. Electronic address: pjli16@glmc.edu.cn.
  • 2 Department of Histology and Embryology, School of Preclinical Medicine, Guilin Medical University, Guilin, Guangxi, PR China; Department of Pathology, Liuzhou People's Hospital, Liuzhou, Guangxi, PR China.
  • 3 Department of Human Anatomy, School of Preclinical Medicine, Guilin Medical University, Guilin, Guangxi, PR China.
  • 4 Department of Clinical Laboratory, Guilin Hospital of the Second Xiangya Hospital CSU, Guilin, Guangxi, PR China.
  • 5 Guangxi Key Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin, Guangxi, PR China; Guangxi Health Commission Key Laboratory of Tumor Immunology and Receptor-Targeted Drug Basic Research, Guilin Medical University, Guilin, Guangxi, PR China. Electronic address: jinfenggan@glmc.edu.cn.
PMID: 38218109 DOI: 10.1016/j.ecoenv.2024.115952
Abstract

Cigarette smoking is one of the most impactful behavior-related risk factors for multiple cancers including hepatocellular carcinoma (HCC). Nicotine, as the principal component of tobacco, is not only responsible for smoking addiction but also a carcinogen; nevertheless, the underlying mechanisms remain unclear. Here we report that nicotine enhances HCC Cancer stemness and malignant progression by upregulating the expression of GC-rich binding factor 2 (GCF2), a gene that was revealed to be upregulated in HCC and whose upregulation predicts poor prognosis, and subsequently activating the Wnt/ꞵ-catenin/SOX2 signaling pathway. We found that nicotine significantly increased GCF2 expression and that silencing of GCF2 reduced nicotine-induced Cancer stemness and progression. Mechanistically, nicotine could stabilize the protein level of GCF2, and then GCF2 could robustly activate its downstream Wnt/β-catenin signaling pathway. Taken together, our results thus suggest that GCF2 is a potential target for a therapeutic strategy against nicotine-promoted HCC.

Keywords

Cancer stem cell; GCF2; HCC; Nicotine; SOX2; Wnt signaling.

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