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RB1 Mutations Induce Smoking-Related Bladder Cancer by Modulating the Cytochrome P450 Pathway.

Zhenguang Mao1,2, Fang Gao1,3, Tuo Sun1,2

  • 1Department of Environmental Genomics and Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China.

Environmental Toxicology
|September 6, 2024
PubMed
Summary
This summary is machine-generated.

Cigarette smoking increases bladder cancer risk by altering the RB1 gene, a key driver. RB1 mutations disrupt cellular functions and the immune microenvironment, promoting tumor growth in smokers.

Keywords:
bladder cancercigarette smoking‐related mutationcytochrome P450 pathwaydriver gene RB1immune microenvironment

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Area of Science:

  • Oncology
  • Genetics
  • Environmental Health

Background:

  • Cigarette smoking is a known carcinogen linked to various cancers, including bladder cancer.
  • The precise mechanisms by which smoking-induced somatic mutations drive bladder tumorigenesis are not fully understood.
  • Understanding these mechanisms is crucial for developing targeted prevention and treatment strategies.

Purpose of the Study:

  • To characterize the smoking-related mutation profile in bladder cancer.
  • To identify smoking-associated driver genes and elucidate their biological mechanisms.
  • To investigate the role of RB1 mutations in smoking-related bladder cancer development.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) cohort for smoking-related mutation profiles.
  • Utilizing the Integrative OncoGenomics database to identify driver genes.
  • Interpretation of biological mechanisms using bulk and single-cell transcriptomics, and cell experiments.
  • Real-time quantitative PCR (RT-qPCR) for gene expression analysis.

Main Results:

  • Cigarette smoking is associated with increased tumor mutational burden in individuals under 65.
  • RB1 was identified as a significantly differentially mutated driver gene in smokers, with a twofold increase in mutation rate.
  • RB1 mutations, influenced by smoking carcinogens like 4-aminobiphenyl, decrease RB1 expression, promoting cancer cell proliferation, invasion, and migration.
  • RB1 mutations were found to inhibit the cytochrome P450 pathway and alter immune cell composition through enhanced cell-cell interactions.

Conclusions:

  • RB1 mutations are a key driver of smoking-related bladder tumorigenesis.
  • Inhibition of the cytochrome P450 pathway and modulation of the tumor immune microenvironment by RB1 mutations contribute to cancer development.
  • This study provides critical insights into the molecular mechanisms linking smoking to bladder cancer.