In this article (Mol Cancer Ther 2010;9:569–80), which appeared in the March 2010 issue of Molecular Cancer Therapeutics (1), the blots of EP3 and EP4 along with the blot of β-actin under Fig. 6B (related with PGE2 receptors part) were incorrectly presented.

Figure 6.

A, dietary GSPs inhibit the growth of A549 and H1299 non–small cell lung cancer cells (NSCLC) grown as xenografts in athymic nude mice (29). Tumor xenografts tissues were harvested at the termination of the experiment, and the wet weight of the tumor/mouse in each group is reported in grams as mean ± SD, n = 10. Statistical significance versus non-GSP–treated controls, *, P < 0.05; , P < 0.01; †, P < 0.001. B, tumor xenograft tissues from control and GSP-treated (0.5%, w/w) mice were used for the analysis of the levels of COX-2 and PGE2 receptors using Western blotting. Dietary GSPs inhibit the levels of COX-2 and PGE2 receptors, EP1, EP3 and EP4, in the tumor xenograft tissues grown in athymic nude mice compared with control tumor xenograft tissues. Representative blots from A549 or H1299 xenografts are presented from the independent analysis of tumors from 6 animals per group with identical results. The relative density (arbitrary) of each band after normalization for β-actin is shown under each immunoblot as the fold change compared with non-GSP–treated control, which was assigned an arbitrary unit 1 in each case. PGE2 was determined in tumor xenograft tissue samples using a PGE2 immunoassay kit following the manufacturer's instructions. The concentration of PGE2 is expressed in terms of pg/mg protein as a mean ± SD, n = 10. Significantly lower versus non-GSP–treated controls. †, P < 0.001.

Figure 6.

A, dietary GSPs inhibit the growth of A549 and H1299 non–small cell lung cancer cells (NSCLC) grown as xenografts in athymic nude mice (29). Tumor xenografts tissues were harvested at the termination of the experiment, and the wet weight of the tumor/mouse in each group is reported in grams as mean ± SD, n = 10. Statistical significance versus non-GSP–treated controls, *, P < 0.05; , P < 0.01; †, P < 0.001. B, tumor xenograft tissues from control and GSP-treated (0.5%, w/w) mice were used for the analysis of the levels of COX-2 and PGE2 receptors using Western blotting. Dietary GSPs inhibit the levels of COX-2 and PGE2 receptors, EP1, EP3 and EP4, in the tumor xenograft tissues grown in athymic nude mice compared with control tumor xenograft tissues. Representative blots from A549 or H1299 xenografts are presented from the independent analysis of tumors from 6 animals per group with identical results. The relative density (arbitrary) of each band after normalization for β-actin is shown under each immunoblot as the fold change compared with non-GSP–treated control, which was assigned an arbitrary unit 1 in each case. PGE2 was determined in tumor xenograft tissue samples using a PGE2 immunoassay kit following the manufacturer's instructions. The concentration of PGE2 is expressed in terms of pg/mg protein as a mean ± SD, n = 10. Significantly lower versus non-GSP–treated controls. †, P < 0.001.

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The experiments were repeated in A549 and H1299 cell lines with and without treatment with grape seed proanthocyanidins (GSP) under identical conditions as used before. Cell lysates were subjected to Western blot analysis for the detection of the levels of PGE2 receptors (EP1, EP3, and EP4), and new data were generated to confirm and verify the levels of PGE2 receptors. The equal protein loading on the gel was verified and re-confirmed using antibody against β-actin. The data obtained re-confirm the results originally reported in the article and thus correct our errors. The authors regret this error.

1.
Sharma
SD
,
Meeran
SM
,
Katiyar
SK
. 
Proanthocyanidins inhibit in vitro and in vivo growth of human non-small cell lung cancer cells by inhibiting the prostaglandin E2 and prostaglandin E2 receptors
.
Mol Cancer Ther
2010
;
9
:
569
80
.