| خلاصه مقاله | Background: Epidemiological studies have suggested that cigaret smoking is associated with increased colorectal cancer (CRC) risk. Nicotine is most likely related to the risk of cigaret smoking and exerts many of its effects on cancer cells through the α7-subtype of nAChR (α7nAChR). The development of CRC originated from cancer stem cells, which comprise a minor population of CRC cells. However, the mechanisms by which nicotine influences the stemness properties of cancer cells are not fully understood.
Materials and Method: To examine the influence of nicotine exposure on cancer stem cell-related gene expression, the present study applied real-time RT-PCR to investigate changes in cancer stem cell-related gene expression in SW-480 CRC cells exposed to nicotine. SW-480 cells were inoculated in 6-well plates to determine the effects of treatments with 1 μM and 10 μM concentrations of nicotine on the expression level of α7nAChR and cancer stem cell markers, including Nanog, Oct-4, Sox-2, CD 44, CD 133, and aldehyde dehydrogenase (ALDH), by quantitative real-time PCR.
Results: The findings showed that nicotine increases the expression of both α7nAChR and cancer stem cell marker mRNA expression. Transfection with α7nAChR-siRNA prevented the observed effects of nicotine, indicating that these effects of nicotine are α7nAChR dependent.
Conclusion: Nicotine has recently been found to enhance the stemness properties of cancer cells. Nicotine alters Nanog, Oct-4, Sox-2, CD 44, CD 133, and ALDH expression in the SW-480 cell line and exerts its effects through the α7nAChR dependent axis. Studying the exact molecular mechanism of nicotine signaling can be useful both in diagnosing and treating nicotine-related cancers and in identifying novel potential therapeutic benefits. |