MCF-7 cells lack the expression of Caspase-3

With great interest, we read the paper Chitosan nano-vehicles as biocompatible delivering tools for a new Ag(I) curcuminoid-Gboxin analog complex in cancer and inflammation therapy published in the International Journal of Biological Macromolecules. In Elbehairi's report, the human breast carcinoma line MCF-7 were used in the in vitro cytotoxic analysis test of the curcuminoid conjugate and its silver(I) complex. They found that Ag(I)FLLL49-GbA could induce highly significant up-regulation of caspase-3, tumor suppressor proteins P53, and Bax after the 48 h of treatment in MCF-7 cells (Fig. 9), and the expression of caspase-3 was analyzed by western blot assay. However, it's well known that the MCF-7 breast carcinoma line do not express caspase-3. The lack of caspase-3 in MCF-7 cells is caused by a 47-base pair deletion within exon 3 of the CASP-3 gene resulting in the skipping of this exon during pre-mRNA splicing and introduction of a premature stop codon at position 42 that completely abrogates translation of the CASP-3 mRNA. Therefore, the detection of a caspase-3 protein in caspase-3 deficient MCF-7 cells in this study made us confused. We appreciate the authors' efforts in investigating the effects of chitosan nano-vehicles as biocompatible delivering tools for a new Ag(I)curcuminoid-Gboxin analog complex in cancer and inflammation therapy. Nevertheless, we sincerely suggest that appropriate modification may further solidify the findings of the study.

Automated summary

In this study, the effects of a new Ag(I)curcuminoid-Gboxin analog complex were investigated using the MCF-7 breast carcinoma cell line. The results showed that Ag(I)FLLL49-GbA could up-regulate the expression of caspase-3, P53, and Bax in MCF-7 cells after 48 hours of treatment. However, it was puzzling because MCF-7 cells do not naturally express caspase-3. Appropriate modifications are suggested to strengthen the findings of this study.