# Effects of Thymoquinone on Cell Proliferation, Oxidative Damage, and Toll-like Signaling Pathway Genes in H1650 Lung Adenocarcinoma Cell Line

## TL;DR

This study explores how thymoquinone affects lung cancer cells by reducing their growth and oxidative stress, but does not significantly impact toll-like receptor gene expression.

## Contribution

The study evaluates the antiproliferative and antioxidant effects of thymoquinone on H1650 lung cancer cells and its impact on toll-like receptor signaling.

## Key findings

- Thymoquinone reduced H1650 cell viability in a time- and dose-dependent manner with an IC50 of 26.59 µM at 48 h.
- Thymoquinone decreased total oxidant status and increased total antioxidant status in H1650 cells.
- No significant changes in TLR gene expressions were observed after thymoquinone treatment.

## Abstract

Background and Objectives: Lung cancer is the leading cause of cancer-related mortality worldwide. In most cases, lung cancer is diagnosed at an advanced stage. For advanced-stage disease, treatment options are generally systemic and while novel treatment approaches offer hope, they may also lead to significant adverse effects. Therefore, alternative therapeutic strategies have been investigated for many years. Thymoquinone (TQ) is one such candidate. Previous studies have demonstrated its antioxidant, anti-inflammatory, antibacterial, and immunomodulatory properties. In our study, we aimed to evaluate the roles of TQ in the progression of H1650 lung adenocarcinoma cells. Materials and Methods: In this study, the antiproliferative effect of TQ on H1650 lung cancer cells was evaluated using MTT assay, its effect on oxidative damage was determined using 8-OHdG, and total antioxidant status (TAS), total oxidant status (TOS), and its effect on apoptosis were demonstrated using caspase-3 ELISA method. In addition, total RNA was extracted from both control and treatment groups, cDNA was synthesized, and mRNA expression changes of Toll-like receptor related genes (TLR) were analyzed using RT-PCR. Results: The decrease in the viability of H1650 lung cancer cells was observed in a time- and dose-dependent manner. The IC50 dose of TQ in the H1650 lung cancer cell line at 48 h was 26.59 µM. TQ treatment decreased the level of TOS and increased the level of TAS in H1650 lung cancer cells. Oxidative stress index decreased in the TQ-treated dose group in H1650 lung cancer cells. Elisa 8-OHdG and caspase-3 levels were not statistically significant. Compared to the control group, no statistically significant changes were observed in TLR1, TLR2, TLR3, TLR4, TLR6, TLR7, TLR8, and TLR9 gene expressions in the treatment group treated with 26.59 µM TQ for 48 h. Conclusions: TQ shows potential as an anticancer agent and may contribute to the development of therapeutic approaches for lung cancers.