Scientists identify new mechanism of prostate cancer cell metabolism

Cancer cell metabolism may present a new target for therapy as scientists have uncovered a possible gene that leads to greater growth of prostate cancer cells.

Study results are published in Cancer Discovery, a journal of the American Association for Cancer Research.

Almut Schulze, Ph.D., a group leader in the Gene Expression Analysis Laboratory at Cancer Research U.K., and colleagues analyzed three metastatic prostate cancer cell lines and compared those findings with those of a nonmalignant prostate epithelial cell line.

"Cancer metabolism is a new and emerging target that can be exploited as a potential therapeutic, and our study identified one of the components for the growth of these cancer cells," she said.

The researchers analyzed the effects of gene silencing of 222 metabolic enzymes, transporters and regulators on the survival of the cell lines.

"This approach revealed a significant complexity in the metabolic requirements of prostate cancer cells and identified genes selectively required for their survival," said Schulze.

Obesity, metabolic syndrome, and prostate cancer Although obesity has been consistently linked to an increased risk of several malignancies, including cancers of the colon, gallbladder, kidney, and pancreas, its role in prostate cancer etiology remains elusive. Data on the association between obesity and prostate cancer incidence are inconsistent, and in some studies obesity is associated with an increase in risk of high-grade prostate cancer but with a decrease in risk of low-grade tumors. In contrast, obesity has been consistently associated with an increased risk of prostate cancer aggressiveness and mortality. The differential effects of obesity on subtypes of prostate cancer suggest etiologic heterogeneity in these tumors and complex interactions between androgen metabolism and several putative risk factors, including insulin resistance, diabetes, inflammation, and genetic susceptibility, on prostate cancer risk. Data on the role of abdominal obesity, insulin resistance, and metabolic syndrome in prostate cancer etiology are limited. Obesity has been shown to be associated with a state of low-grade chronic inflammation, and insulin resistance and the metabolic syndrome are associated with adverse metabolic profiles and with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor-, many of which have been shown to enhance tumor growth. Thus, whether obesity and metabolic syndrome modulate the risk of prostate cancer through chronic inflammation needs to be investigated further. Given that the prevalence of obesity and metabolic syndrome is increasing worldwide and that the world population is aging, the roles of obesity and metabolic syndrome in prostate carcinogenesis warrant further clarification.

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Hsing AW, Sakoda LC, Chua S Jr.Source: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20852-7234, USA. [email protected]