and anti-leukemic activity of 2-amino-6-nitro-4-(4-oxo-2-thioxothiazolidin-5-yl)-4H-chromene-3-carbonitrile (ANC) through inhibition of anti-apoptotic Bcl-2 proteins.

An array of 4H-chromene derivatives have been reported for anticancer properties but their selectivity and mode of anticancer activity are unexplored. In this context, we have investigated a biologically active synthetically designed 4H-Chromene carbonitrile derivative, 2-amino-6-nitro-4-(4-oxo-2-thioxothiazolidin-5-yl)-4H-chromene-3-carbonitrile (ANC) that is strongly and selectively inhibited Bcl-2 over expressing human leukemic (HL-60 and K562) cells for its interaction and elucidated the mode of action. The interaction of ANC was investigated against the antiapoptotic proteins such as Bcl-2, Bax, Bcl-xL and Bcl-w that were overexpressed in leukemic cells using and fluorescent spectroscopic studies.

Anti-leukemic, anti-lung, and anti-breast cancer potential of the microbial polyketide 2, 4-diacetylphloroglucinol (DAPG) and its interaction with the metastatic proteins than the antiapoptotic Bcl-2 proteins.

The microbial polyketide, 2, 4-diacetylphloroglucinol (DAPG), exhibited a broad-spectrum of anti-leukemic, anti-lung, and anti-breast cancer properties. The aim of the present investigation was to study the interactive potentials of DAPG with the metastatic proteins such as MMP-2, MMP-9, and NF-κB and antiapoptotic Bcl-2 family proteins such as Bcl-2, Bcl-w, and Bcl-xL through in silico interaction and in vitro studies. The in silico modeling predicted high interactions of DAPG with the metastatic proteins, especially MMP-2, MMP-9, and NF-κB with the glide score of -7.

In vitro antiproliferative, pro-apoptotic, antimetastatic and anti-inflammatory potential of 2,4-diacetylphloroglucinol (DAPG) by Pseudomonas aeruginosa strain FP10.

The 2,4-diacetylphloroglucinol (DAPG), a polyketide metabolite extracted from Pseudomonas aeruginosa strain FP10, exhibited selective cytoxicity against lung (A549), breast (MDA MB-231), cervical (HeLa) and colon (HCT-15) cancer cells in differential and dose-dependent manner. The anticancer and antimetastatic activities of DAPG were mediated by the inhibition of ROS, NF-κB, Bcl-2, MMP-2, VEGF and primary inflammatory mediators such as TNF-α, IL-6, IL-1β and NO. The DAPG induced apoptosis in cancer cells by intrinsic and extrinsic pathways via the release of cytochrome-C, upregulation of Bax and the activation of caspases and also, exhibited anti-inflammatory activity by the inhibition of LPS-inflammed cell proliferation of macrophage (Raw 264.