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View the Table of Contents for the January 2008 issue of Molecular Cancer Therapeutics
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The PRL phosphatases are currently being investigated as potential therapeutic targets in cancer. However, the expression of PRL phosphatases in pancreatic cancer and the effects of PRL protein inhibition in pancreatic cancer cells have not been explored. Stephens and colleagues found that both PRL-1 and PRL-2, but not PRL-3 are potentially overexpressed in pancreatic cancer, and siRNA mediated knockdown of both PRL-1 and PRL-2 was needed to see anti-tumorigenic effects. Their data suggested that all three PRL proteins should be evaluated in future PRL studies, and that PRL phosphatases might perform similar functions upstream of AKT in cancer cells.
Prislei et al. Page 233 Overexpression of class III β-tubulin (TUBB3) represents a prominent mechanism of drug resistance in several solid tumors. Prislei and colleagues found a novel pathway linked to the control of TUBB3 expression. TUBB3 expression was either enhanced or inhibited if semaphorin 6 class A (SEMA6A) was stably overexpressed or silenced, respectively. This mechanism was associated with SEMA6A cytoskeletal compartmentalization, in a complex with β-actin. The authors concluded that SEMA6A cytoskeletal signaling function is distinct from the known role as a membrane receptor and provides a novel “druggable” target, useful to circumvent TUBB3 overexpression and the consequent acquisition of the drug resistant phenotype.
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