Naphthoquinone components from Alkanna tinctoria (L.) Tausch show significant antiproliferative effects on human colorectal cancer cells

Abstract

Our research to seek active compounds against human colorectal cancer from the root of Alkanna tinctoria (L.) Tausch led to the isolation of two naphthoquinones, alkannin (1) and angelylalkannin (2). The antiproliferative effects of the two compounds on human colon cancer cells HCT-116 and SW-480 were determined by the 3,4-(5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt (MTS) method. Cell cycle profile and cell apoptosis were determined using flow cytometry. Both of the two compounds showed significant inhibitory effects on the cancer cells. For alkannin (1) and angelylalkannin (2), the median inhibitory concentration (IC₅₀) values were 2.38 and 4.76 µM for HCT-116 cells, while for SW-480 cells they were 4.53 and 7.03 µM, respectively. The potential antiproliferative mechanisms were also explored. At concentrations between 1-10 µM, both compounds arrested the cell cycle at the G1 phase and induced cell apoptosis.

Figure 1

The structures of alkannin (1) and angelylalkannin (2).

Figure 2

Antiproliferative effects of alkannin (1) and angelylalkannin (2) on human colorectal cancer cells. HCT-116 and SW-480 cells were treated with the compounds at various concentrations for 48 h. Cell proliferation was determined using MTS method. Data are presented as mean ± standard error. *, P<0.05; **, P<0.01 vs. control.

Figure 3

Effects of alkannin (1) and angelylalkannin (2) on HCT-116 cell cycle. HCT-116 cells were treated with 1 and 3 µM of the compounds for 48 h. Cell cycle profile was determined using flow cytometry after staining with PI/RNase. Percentages of cells in G1, S and G2/M phases are indicated.

Figure 4

Effects of alkannin (1) and angelylalkannin (2) on HCT-116 cell apoptosis. HCT-116 cells were treated with 1, 3, and 10 µM of the compounds for 48 h. Apoptosis was quantified using flow cytometry after staining with annexin V/PI.