期刊
CANCER INVESTIGATION
卷 27, 期 4, 页码 417-429出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/07357900802438585
关键词
Apoptosis; Caspase; Paclitaxel; Temporal response; Drug resistance
类别
资金
- 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
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.
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