Luteolin alters MUC1 extracellular domain, sT antigen, ADAM‑17, IL‑8, IL‑10 and NF‑κB expression in <i>Helicobacter</i> <i>pylori</i>‑infected gastric cancer CRL‑1739 cells: A preliminary study
Iwona Radziejewska, Małgorzata Borzym‐Κluczyk, Katarzyna Leszczyńska
Abstract
Luteolin is a natural flavonoid possessing certain beneficial pharmacological properties, including anti‑oxidant, anti‑inflammatory, anti‑microbial and anti‑cancer properties. The majority of types of gastric cancer with chronic gastritis are caused by infection with <em>Helicobacter pylori</em> (<em>H. pylori</em>). The present study evaluated the effect of luteolin on a number of selected factors that are potentially involved in gastric cancer development. The study was performed using gastric cancer CRL‑1739 cells treated with 30 <em>µ</em>M luteolin and <em>H. pylori</em> alone or combined. ELISA and reverse transcription PCR were used to assess the expression levels of MUC1, GalNAcα‑R (Tn antigen) and NeuAcα2‑3Galβ1‑3GalNAc‑R (sT antigen), ADAM‑17, IL‑8, IL‑10 and NF‑κB. <em>H. pylori</em> and luteolin independently and in combination significantly reduced the expression levels of the extracellular domain of MUC1 in gastric cancer cells compared with the untreated control cells. ADAM‑17 expression was reduced by treatment with the pathogen and luteolin. Additionally, both factors reduced sT antigen expression. Treatment with 30 ≤M luteolin significantly induced IL‑8 expression at the mRNA and protein level, and the mRNA expression levels of IL‑10 and NF‑κB compared with the control. Both <em>H. pylori</em> and luteolin induced IL‑8 protein expression. The present preliminary results suggest that luteolin may be used to treat patients with gastric cancer.