Abstract
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.
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