B6190
Description:
IC50: 1.7-4.0 μM for tested cancer cell lines
NSC348884 is a nucleophosmin inhibitor.
Nucleophosmin is identified as a multifunctional nucleolar phosphoprotein, which is dysregulated in human malignancies resulting in anti-apoptosis and differentiation inhibition.
In vitro: NSC348884, which was identified as a putative nucleophosmin small molecular inhibitor, was found to be able to disrupt a hydrophobic pocket that was required for oligomerization, and NSC348884 could also inhibit the cell proliferation in distinct cancer cell lines and disrupt nucleophosmin oligomer formation. Moreover, the treatment of several cancer cell types with NSC348884 could dose-dependently upregulate p53 and also induce apoptosis that correlated with H2AX phosphorylation, poly(ADP-ribose) polymerase cleavage as well as Annexin V. Furthermore, NSC348884 could also synergize doxorubicin cytotoxicity on the viability of cancer cells [1]. …show more content…
In addition, there was no significant difference in overall cell death that was observed by histology in the treated tumors with the 4-hour brief treatments, indicating that the inhibition seen was specific to migration
Description:
IC50: 1.7-4.0 μM for tested cancer cell lines
NSC348884 is a nucleophosmin inhibitor.
Nucleophosmin is identified as a multifunctional nucleolar phosphoprotein, which is dysregulated in human malignancies resulting in anti-apoptosis and differentiation inhibition.
In vitro: NSC348884, which was identified as a putative nucleophosmin small molecular inhibitor, was found to be able to disrupt a hydrophobic pocket that was required for oligomerization, and NSC348884 could also inhibit the cell proliferation in distinct cancer cell lines and disrupt nucleophosmin oligomer formation. Moreover, the treatment of several cancer cell types with NSC348884 could dose-dependently upregulate p53 and also induce apoptosis that correlated with H2AX phosphorylation, poly(ADP-ribose) polymerase cleavage as well as Annexin V. Furthermore, NSC348884 could also synergize doxorubicin cytotoxicity on the viability of cancer cells [1]. …show more content…
In addition, there was no significant difference in overall cell death that was observed by histology in the treated tumors with the 4-hour brief treatments, indicating that the inhibition seen was specific to migration