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Poster Display session

210P - Expression of cancer stem cell markers SOX-2 and OCT-4 and their regulation by nicotine in non-small cell lung carcinoma

Date

31 Mar 2023

Session

Poster Display session

Presenters

Jayanthi Pazhani

Citation

Journal of Thoracic Oncology (2023) 18 (4S): S149-S153.
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Authors

J. Pazhani1, V.P. Veeraraghavan2, S. Jayaraman3, M. El-Sherbiny4, A.M. Ali Hakami4, A. Mousaed Almotairi4, H.A. Ebrahim5

Author affiliations

  • 1 Chennnai/IN
  • 2 Saveetha Institute of Medical and Technical Sciences, Chennnai/IN
  • 3 SIMATS - Saveetha Institute of Medical and Technical Sciences, Poonamallee/IN
  • 4 College of Medicine, AlMaarefa University, Riyadh/SA
  • 5 Princess Nourah bint Abdulrahman University, Riyadh/SA

Resources

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Abstract 210P

Background

Lung cancer remains one of the leading causes of cancer-related death worldwide and approximately 80% of lung cancers are non-small cell lung carcinomas (NSCLC). The incidence of lung cancer is highly correlated with cigarette smoking and nicotine is the addictive component of tobacco smoke. Nicotine can promote proliferation, migration, and invasion of cells in vitro and promote tumor growth and metastasis in vivo through activation of nicotine acetylcholine receptors. Recently, nicotine is implicated in promoting self-renewal of cancer stem cells in lung cancer. Cancer stem cells (CSC) are a subset of tumor cells that has the ability to self-renew and generate tumor heterogeneity leading to tumor progression and invasion. This study was done to evaluate the expression of CSC markers SOX-2 and OCT-4 in NSCLC and their regulation by nicotine.

Methods

Tissue samples were collected from 40 histopathologically confirmed cases of NSCLC and expression of SOX-2 and OCT-4 was evaluated using immunohistochemistry. The mean immunoreactive score (staining intensity x proportion of positive cells) was calculated and compared between tumor tissue and adjacent normal lung tissue. The immunohistochemical expressions of SOX-2 and OCT-4 were also correlated with clinicopathological parameters such as age, gender, tobacco habit and histopathological grade of the tumor. Experiments were conducted using A549 human lung adenocarcinoma cell lines, where cells were serum starved for 24 hrs and stimulated with 2 μM nicotine. The induction of SOX-2 was examined using immunofluroscence microscopy.

Results

The mean immunoreactive score of SOX-2 and OCT-4 was higher in tumor tissues compared to adjacent normal tissue in patients with NSCLC Higher expression of CSC markers was noticed in tobacco habituates (p = 0.001) and in poorly differentiated tumors (p = 0.01). SOX-2 was found to be induced after 21 hours of nicotine stimulation in A549 lung cancer cells.

Conclusions

Our findings shed light on novel molecular mechanisms underlying the pathophysiology of smoking- related lung cancer in the context of cancer stem cell populations, and reveal new pathways involved that could potentially be exploited therapeutically.

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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