The cannabinoids may be useful to ER- but not ER+.
Although they don't seem to know how to target Metadherin directly, some of the pathways it triggers seem to be familiar and have various potential blockers:
Clin Cancer Res. 2009 Sep 15;15(18):5615-20. Epub 2009 Sep 1.
The multifaceted role of MTDH/AEG-1 in cancer progression.
Hu G,
Wei Y,
Kang Y.
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.
Cancer is the result of the progressive acquisition of multiple malignant traits through the accumulation of genetic or epigenetic alterations. Recent studies have established a functional role of MTDH (Metadherin)/AEG-1 (Astrocyte Elevated Gene 1) in several crucial aspects of tumor progression, including transformation, evasion of apoptosis, invasion, metastasis, and chemoresistance. Overexpression of MTDH/AEG-1 is frequently observed in melanoma, glioma, neuroblastoma, and carcinomas of breast, prostate, liver, and esophagus and is correlated with poor clinical outcomes. MTDH/AEG-1 functions as a downstream mediator of the transforming activity of oncogenic Ha-Ras and c-Myc. Furthermore, MTDH/AEG-1 overexpression activates the PI3K/Akt, nuclear factor kappaB (NFkappaB), and Wnt/beta-catenin signaling pathways to stimulate proliferation, invasion, cell survival, and chemoresistance. The lung-homing domain of MTDH/AEG-1 also mediates the adhesion of tumor cells to the vasculature of distant organs and promotes metastasis. These findings suggest that therapeutic targeting of MTDH/AEG-1 may simultaneously suppress tumor growth, block metastasis, and enhance the efficacy of chemotherapeutic treatments.
PMID: 19723648 [PubMed - in process]