Compound_ID |
Target |
Gene_Name |
Gene_ID |
Cancer |
Cell_lines |
IC50 Value |
EC50 Value |
ED50 Value |
GI50 Value |
Remarks |
References |
MMP-AC0211 |
BAX |
BCL2-associated X protein |
581 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
Pinocembrin (100 mµM) induced Bax translocation to mitochondria. Overexpression of Bax sensitized cells to pinocembrin-induced apoptosis as evidenced from MTT and chromatin condensation. |
17186548 |
MMP-AC0211 |
BAX |
BCL2-associated X protein |
581 |
Neuroblastoma |
SH-SY5Y |
- |
- |
- |
- |
Pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax-Bcl-2 ratio. |
18625218 |
MMP-AC0211 |
BCL2L1 |
BCL2-like 1 |
598 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
Here,it is indicated that cytochrome c release induced by pinocembrin is not blocked by Bcl-XL. And overexpression of Bcl-XL only partially prevented chromatin condensation and cytochrome c release induced by pinocembrin compared to vector-transfected cells. |
17186548 |
MMP-AC0211 |
CASP3 |
caspase 3, apoptosis-related cysteine peptidase |
836 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
The processing of caspase-3 was evident from 24 h of pinocembrin treatment and by 48 hmore intense cleavage fragment was evident. Caspase-3 inhibitor reduced the chromatin condensation to 15%, compared to 30% in DMSO control. |
17186548 |
MMP-AC0211 |
CASP9 |
caspase 9, apoptosis-related cysteine peptidase |
842 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
Caspase-9 was cleaved to its cleavage fragment (37 kDa) after 48 h of pinocembrin treatment.Pinocembrin-induced caspase-9 processing is subsequent to loss of mitochondrial membrane permeabilization and release of cytochrome c into cytosol, indicating a possible role for classical mitochondrial apoptotic signaling. Caspase-9 inhibitor reduced the chromatin condensation to 18%, compared to 30% in DMSO control. |
17186548 |
MMP-AC0211 |
CYCS |
cytochrome c |
54205 |
Neuroblastoma |
SH-SY5Y |
- |
- |
- |
- |
Pinocembrin inhibit the release of cytochrome c from mitochondria to cytosol. |
18625218 |
MMP-AC0211 |
CYCS |
cytochrome c |
54205 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
The release of cytochrome c is essential for the processing of initiator caspase-9 in mitochondria-mediated apoptotic signaling. The release of cytochrome c in to cytosol began after 24 h of pinocembrin and gradually increased to 72 h. |
17186548 |
MMP-AC0211 |
PARP1 |
poly (ADP-ribose) polymerase 1 |
142 |
Colon cancer |
HCT-116 |
- |
- |
- |
- |
PARP is an important enzyme responsible for the DNA repair and is a preferred substrate for processed caspase-7 and -3.Western blot analysis of treated samples shows that cleavage of PARP is evident only around 48 h of drug exposure. |
17186548 |
MMP-AC0211 |
TP53 |
tumor protein p53 |
7157 |
Neuroblastoma |
SH-SY5Y |
- |
- |
- |
- |
Pinocembrin could also down-regulate the expression of p53 protein, and inhibit the release of cytochrome c from mitochondria to cytosol. |
18625218 |