A potential treatment target for metastatic cancers.
Nearly all deaths caused by solid cancers are due to the occurrence of metastases, secondary tumors that emerge in distant organs such as the lungs, liver, brain and bone. Although it is already well established that growth factors such as members of the epidermal growth factor signaling pathway propel cell migration and metastasis, the underlying molecular mechanisms are still incompletely understood. In the clinical perspective, the efficacy of current anti-cancer treatments such as classical chemotherapies and molecularly targeted drugs has been demonstrated on primary cancers, but their utility as anti-metastatic agents remains limited. Thus, a major unmet need exists for innovative anti-metastatic therapies that block malignant cells from acquiring metastatic potential, while reducing harmful effects inflicted on healthy cells. The present technology provides means to specifically target a recently identified key metastasis-driving gene. The same technology also allows for the development of new tools to detect, prognose and treat metastatic disease.
Inhibition of tumor metastasis and invasiveness by downregulation of SYNJ2 expression.
- SYNJ2 inhibition can be realized either as a single-agent therapy, or as part of combination regimens alongside chemotherapeutic agents or molecularly targeted drugs.
- Assessment of SYNJ2 levels in patients may be utilized as a multimodal biomarker for therapy outcome, prognosis and diagnosis.
- The processing of SYNJ2 may serve as a functional output in a screening platform to identify putative tumor metastasis inhibitors.
- Targeted cancer therapies will give doctors a better way to tailor cancer treatment.
- Modulation of SYNJ2 may lead to increased efficacy with potentially fewer adverse side effects.
Weizmann Institute researchers have uncovered an essential component in the metastatic process of cancerous cells. The innovators have shown that the EGF-inducible lipid phosphatase, Synaptojanin 2 (SYNJ2), is a master promoter of invadopodia formation and breast cancer metastasis. Proof-of-concept studies performed in preclinical animal models demonstrated that SYNJ2 inhibition led to tumor burden reduction and diminished metastatic spread, indicating that SYNJ2 inhibitors may be employed as a promising anti-cancer and anti-metastatic agents. Moreover, molecular profiling studies have uncovered that SYNJ2 expression is associated with human breast tumor aggressiveness, further suggesting SYNJ2 utility as a marker for cancer diagnosis, prognosis and treatment outcome.