Abstract
The “oncogene addiction” concept refers to the dependence of cancer cells on the function of the oncogenes responsible for their transformed phenotype, while the term “non-oncogene addiction” has been introduced to define the exacerbated necessity of the normal function of non-mutated genes. In this Perspective, we focus on the importance of proteolytic enzymes to maintain the viability of cancer cells and hypothesize that most, if not all, tumors present “addiction” to a number of proteolytic activities, which in turn may represent valuable targets of anti-cancer therapies, even without being mutated or over-expressed by the malignant cells.
Highlights
The “oncogene addiction” concept refers to the dependence of cancer cells on the function of the oncogenes responsible for their transformed phenotype, while the term “non-oncogene addiction” has been introduced to define the exacerbated necessity of the normal function of non-mutated genes
Ron DePinho and colleagues reported that oncogenic H-Ras is essential for tumor maintenance in a doxycyclineinducible H-RasV12G mouse melanoma model null for the tumor suppressor INK4a, as downregulation of the oncogene resulted in tumor regression (Chin et al, 1999)
The induction of the oncogene led to development of lung adenocarcinomas, which underwent apoptotic regression upon removal of the inductor, demonstrating that the function of this oncogene is necessary to maintain the viability of tumor cells even in the absence of key tumor suppressors such as p53 or Ink4A (Fisher et al, 2001)
Summary
The “oncogene addiction” concept refers to the dependence of cancer cells on the function of the oncogenes responsible for their transformed phenotype, while the term “non-oncogene addiction” has been introduced to define the exacerbated necessity of the normal function of non-mutated genes. Oncogene addiction In line with the multiple efforts to develop more efficient and selective therapies based on targeting tumor-specific traits, the concept of “oncogene addiction” was introduced to emphasize the apparent dependency of cancer cells on one or a few genes for the maintenance of the malignant phenotype (Weinstein, 2002; Weinstein and Joe, 2006, 2008).
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