Abstract

Purpose : To evaluate the anti-cancer activity of Indonesian Pasuruan propolis extract (PPE) against HT-29 human colon carcinoma cell line. Methods : HT-29 cells were cultured and treated in different concentrations of PPE (50, 100, 200, 400 μg/mL) for 24 h. The cells were evaluated by several indicators such as cell proliferation and apoptosis as well as the expression of protein Ki67, p53, cyclin D1, and Bcl-xL. Results : Administration of PPE inhibited cell proliferation of HT-29 in concentration-dependent manner but the effect was not significant (p = 0.842); the results were similar with regard to the expression of Ki67 in HT-29 cells (p = 0.953). Administration of 400 μg/mL PPE insignificantly decreased cyclin D1 expression (p = 0.149). The concentration of PPE at 50, 100, and 200 μg/mL induced cell apoptosis of HT-29 cells initially, but the level of apoptosis subsequently decreased (p = 0.416). Furthermore, the expressions of p53 and Bcl-xL decreased following treatment with PPE at 50, 100 and 200 μg/mL but increased for the PPE 400 μg/mL group (p = 0.000). Conclusion : PPE reduced the expressions of p53, Ki67, cyclin D1, and Bcl-xL insignificantly as it it generally failed inhibit cell proliferation and promote cell apoptosis of HT-29 cells. Keywords : Bcl-xL, Colon cancer, Cyclin D1, Human colon adenocarcinoma cell line HT-29, Proliferation marker Ki67, Tumor protein p53

Highlights

  • Colorectal cancer (CRC) contributed the third highest cancer prevalence in men and the second highest in women worldwide

  • It has been reported that the inactivity of p53 protein is possibly leads to TP53 gene mutation. p53 mutation occurs in approximately 40-50 % of sporadic CRC

  • This research aimed to observe the effect of Indonesian Pasuruan propolis extract (PPE) against HT-29 human colon carcinoma cell line by inhibiting the cell cycle and promoting the expression of apoptotic markers including p53, Ki67, cyclin D1 and Bcl-xL

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Summary

Introduction

Colorectal cancer (CRC) contributed the third highest cancer prevalence in men and the second highest in women worldwide. More efficacious approaches are urgently needed for CRC patient. It has been reported that the inactivity of p53 protein is possibly leads to TP53 gene mutation. P53 mutation occurs in approximately 40-50 % of sporadic CRC. CRC patients with mutant p53 appear to be more chemo-resistant and have poorer prognosis than those with the wild-type [2]. This protein protecting genome from changes as the result of DNA damage by stopping cell cycle and inducing the activation of cell repair mechanisms, as well as cell death [3]. The activation of p53 protein by stress factors will enter into the mitochondria to activate the expression of pro-apoptotic genes, as well as inhibits the expression of anti-apoptotic genes, such as those of the Bcl family -2 (Bcl-2, Bcl-X, Bcl-in, Mcl-1) [3]

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