gms | German Medical Science

Objective: Adiponectin (Acrp30), a 30-kDa component C1q-related protein, is an adipocyte-secreted hormone that plays an important role in the development and progression of several malignancies. Recent in vitro studies demonstrate the antiangiogenic and tumor growth-limiting properties of adiponectin. Studies in both animals and humans have investigated adiponectin and adiponectin receptor regulation and expression in several cancers types. Many different cancer cell types express the signaling of AdipoR1 and respond to adiponectin. The role of the Adiponectin/AdipoR system in human cerebral neoplasms remains unclear. The potential involvement of the system in glioblastoma has been already discussed in recent published data. In summary, our data demonstrate that the adiponectin system is expressed not only in malignant brain tumors such as glioma but also in meningeomas. Also Leptin, a 16 kDa polypeptidic hormone synthesized essentially by adipose tissue, was first described as a regulator of body weight and energy balance. Furthermore, leptin can activate migration and invasion, and is a potent angiogenic factor acting independently or through upregulation of vascular endothelial growth factor. In addition, leptin can amplify some oncogenic pathways via transactivation of receptors for epidermal growth factor and insulin like growth factor I. We examined the expression of leptin receptor (Ob-R) in human meningioma.

Methods: Series of frozen surgical samples derived from malignant intracranial tumors and proteins from meningeomas cell lines lysates were size-fractionated and analyzed by real time PCR and Western blot (WB).

Results: The expression of Adipo R1 was evaluated by real time PCR and confirmed WB in protein lysates. The expression of both Adipo-R1 was weakly positive in benign meningioma, bronchial- and breast caner, but was considerably increased in aggressive forms of meningioma, oligodendroglioma and glioblastoma, where the labeling was the most intense. The expression of Leprtin-Receptors was evaluated by WB in protein lysates. The expression of Leptin-Receptor was negative in benign meningioma, but was overexpressed in aggressive forms of meningioma and malignant brain tumors.

Conclusion: The present study shows clear evidence for an expression of Adiponectin/AdipoR1 in both benigne and malign neoplasms of the brain. Both markers were highly expressed in glioblastoma, oligodendroglioma and high-grade meningioma, while lower expression of Adiponectin/AdipoR1 was noted in low-grade meningioma and metastasis. The relationship between the adiponectin system and the development of primary neoplasms of the brain remains unclear. The potential role of leptin in human brain tumors has never been explored. It has been shown the leptin and ObR mRNA expression in various intracranial tumors. We showed the expression of Leptin-Receptor was negative in benign meningioma, but was overexpressed in aggressive forms of meningioma and malignant brain tumors. We therefore recommend further in-vivo as well as in-vitro investigation to unveil possible beneficial values of the Adiponectin/AdipoR system and of the leptin/leptin-receptors for the diagnosis and treatment of cerebral tumors.