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Obesity is a significant risk factor for post-menopausal women to developand die from breast cancer. Leptin, an adipokine is produced in high levels inobese individuals, and its receptor is overexpressed in breast tumors and lymphnode metastases. Previously, we demonstrated that leptin stimulates breast cancercell invasion, which is correlated with breast cancer metastasis. Programmed celldeath 4 (PDCD4) has been shown to block cancer cell invasion. However, whetherPDCD4 blocks leptin-induced breast cancer cell invasion is not known. Here, wereport the novel findings that leptin failed to induce invasion in MCF-7 breastcancer cells overexpressing PDCD4 (MCF-7/PDCD4). Tissue inhibitor of metalloproteinase-2(TIMP-2) was essential to the anti-invasive effect of PDCD4, as leptin stimulatedthe invasion of MCF-7/PDCD4 cells pretreated with TIMP-2 siRNA. Furthermore, TIMP-2knockdown allowed leptin to augment phosphorylation of extracellular signal-regulatedkinases 1,2 and signal transducer and activator of transcription 3, but not thatof Jun N-terminal kinases. These data indicate that PDCD4 utilizes TIMP-2 to exertits anti-invasive effect by suppressing leptin-induced activation of extracellularsignal-regulated kinases 1,2 and signal transducer and activator of transcription3. Novel therapeutic strategies aiming at enhancing PDCD4 expression in breasttumors may be able to stop obesity-related breast tumor progression and prolongthe life of patients.

Programmed cell death 4 inhibits leptin-induced breast cancer cell invasion