Journal
CANCER INVESTIGATION
Volume 27, Issue 4, Pages 417-429Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/07357900802438585
Keywords
Apoptosis; Caspase; Paclitaxel; Temporal response; Drug resistance
Categories
Funding
- NCI Cancer Center [P30 CA91842]
- NIH [R01 CA109754, R01 EB1430, R33 CA100972, R21 CA123537]
- NATIONAL CANCER INSTITUTE [P30CA091842, R21CA100972, R21CA123537, R01CA109754, R33CA123537, R33CA100972] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [R01EB001430] Funding Source: NIH RePORTER
Ask authors/readers for more resources
In spite of compelling evidence-implicating caspases in drug-induced apoptosis, how tumors modulate caspase expression and activity to overcome the cytotoxicity of anticancer agents is not fully understood. To address this issue, we investigated the role of caspases-3 and caspase-7 in determining the response of breast and lung tumor cell lines to chemotherapy. We found that an early and late apoptotic response correlated with weak and strong cellular caspase-activation, respectively. The results highlight an underappreciated relationship of temporal apoptotic response with caspase-activation and drug resistance. Moreover, the extent of tumor growth restoration after drug withdrawal was dependent on the degree of endogenous blockage of caspase-3 and caspase-7 cleavages. This points to an unrecognized role of caspase modulation in tumor recurrence and suggests that targeting caspase cleavage is a rational approach to increasing potency of cancer drugs.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available