TY - JOUR
T1 - Identification of a potent herbal molecule for the treatment of breast cancer
AU - Koduru, Srinivas
AU - Sowmyalakshmi, Srinivasan
AU - Kumar, Raj
AU - Gomathinayagam, Rohini
AU - Rohr, Jürgen
AU - Damodaran, Chendil
N1 - Funding Information:
This work was supported by the grant from the Susan G. Komen Breast Cancer Foundation to CD.
PY - 2009/1/30
Y1 - 2009/1/30
N2 - Background: Breast cancer (BCa)-related mortality still remains the second leading cause of cancer-related deaths worldwide. Patients with BCa have increasingly shown resistance and high toxicity to current chemotherapeutic drugs for which identification of novel targeted therapies are required. Methods: To determine the effect of PDBD on BCa cells, estrogen-receptor positive (ER+)-MCF-7 and estrogen-receptor negative (ER-)-MDA 231 cells were treated with PDBD and the cell viability, apoptotic, cell cycle, Western blot and Promoter assays were performed. Results: PDBD inhibitscell viability of ER+ and ER- BCa cells by inducing apoptosis without causing significant toxicity in normal breast epithelial cells. While dissecting the mechanism of action of PDBD on BCa, we found that PDBD inhibits Akt signaling and its downstream targets such as NF-κB activation, IAP proteins and Bcl-2 expression. On the other hand, activation of JNK/p38 MAPK-mediated pro-apoptotic signaling was observed in both ER+ and ER- BCa cells. Conclusion: These findings suggest that PDBD may have wide therapeutic application in the treatment of BCa.
AB - Background: Breast cancer (BCa)-related mortality still remains the second leading cause of cancer-related deaths worldwide. Patients with BCa have increasingly shown resistance and high toxicity to current chemotherapeutic drugs for which identification of novel targeted therapies are required. Methods: To determine the effect of PDBD on BCa cells, estrogen-receptor positive (ER+)-MCF-7 and estrogen-receptor negative (ER-)-MDA 231 cells were treated with PDBD and the cell viability, apoptotic, cell cycle, Western blot and Promoter assays were performed. Results: PDBD inhibitscell viability of ER+ and ER- BCa cells by inducing apoptosis without causing significant toxicity in normal breast epithelial cells. While dissecting the mechanism of action of PDBD on BCa, we found that PDBD inhibits Akt signaling and its downstream targets such as NF-κB activation, IAP proteins and Bcl-2 expression. On the other hand, activation of JNK/p38 MAPK-mediated pro-apoptotic signaling was observed in both ER+ and ER- BCa cells. Conclusion: These findings suggest that PDBD may have wide therapeutic application in the treatment of BCa.
UR - http://www.scopus.com/inward/record.url?scp=61749093641&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=61749093641&partnerID=8YFLogxK
U2 - 10.1186/1471-2407-9-41
DO - 10.1186/1471-2407-9-41
M3 - Article
C2 - 19183448
AN - SCOPUS:61749093641
SN - 1471-2407
VL - 9
JO - BMC Cancer
JF - BMC Cancer
M1 - 41
ER -