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Blocking anti‐apoptosis as a strategy for cancer chemotherapy: NF‐κB as a target
Author(s) -
Monks N.R.,
Biswas D.K.,
Pardee A.B.
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20080
Subject(s) - apoptosis , cancer research , cancer cell , biology , estrogen receptor , programmed cell death , cancer , microbiology and biotechnology , breast cancer , biochemistry , genetics
Abstract Critical processes underlying cancers must be better understood to develop strategies for treatment and prevention. A chemotherapeutic strategy is proposed that is based upon re‐establishment, with a drug, of nullified programmed cell death (apoptosis) in cancer cells, which to survive have mutated to block apoptosis. A chemotherapy that is specific against tumors implanted in mice demonstrated the feasibility of this principle. This therapy is specific because it affects a process unique to cancer cells. It also has the advantage of killing these cells, in contrast to reversibly blocking their proliferation. The anti‐apoptotic transcription factor NF‐κB provides a potential therapeutic target in estrogen receptor negative (ER−) breast cancers that over‐express the epidermal growth factor family of receptors (EGFR). Further investigations of the pathways utilize dominant negative protein inhibitory peptide, and small inhibitory RNAs (siRNAs) to block the production of relevant enzymes. © 2004 Wiley‐Liss, Inc.