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According to a study appearing in the journal Cell Reports, silencing a protein called SIRT2 could a therapeutic strategy to the deadliest form of breast cancer. CusAb-Flarebio offers SIRT2, HER2, Slug and Recombinant ITGB1

In the past decade, much progress has been made in the treatment of breast cancer. For most forms of breast cancer, tailored targeted therapies can improve patients' survival. However, a more aggressive form of breast cancer, called basal-like breast cancer (BLBC), is still difficult to treat. BLBC accounts for about 20% of all cases of breast cancer and it is typically triple-negative, which means that the tumors do not express estrogen receptor, progesterone receptor, and HER2. Furthermore, BLBC tumors are highly invasive and are often resistant to traditional treatments. Currently, there is no promising target for therapeutic intervention of this deadly form of breast cancer.

Now, a newest study shows that inactivating SIRT2 can decrease the invasiveness of BLBC because SIRT2 loss improves the degradation of Slug, a protein that is critical for tumor progression and metastasis. The study, carried out by scientists at Tufts University School of Medicine and other collaborators, is an important step toward understanding the mechanisms of BLBC and discovering new drug targets.

Slug, a transcription factor, is well known to promote tumor progression and metastasis, causing loss of cell adhesion as well as invasive properties. In many BLBC tumors, the Slug protein is overabundant. Scientists have already shown that blocking Slug decreases the invasiveness of tumors. But targeting a transcription factor is not easy.

To find novel targets for the treatment of BLBC, Dr Charlotte Kuperwasser and colleagues at Tufts University School of Medicine investigated what control Slug abundance. They revealed that SIRT2, which is a member of the sirtuin family of enzymes, plays a central role in regulating Slug stability. When the researchers inactivated SIRT2 in BLBC tumor cells, the degradation of Slug was accelerated. Furthermore, the SIRT2-depleted tumor cells had reduced capacity for invasiveness, growth and self-renewal. On the other hand, adding Slug protein back to these cells resulted in invasive traits.

Furthermore, Dr Kuperwasser also found SIRT2-depleted tumor cells formed smaller tumors in mice. These results demonstrated that SIRT2 is associated with both Slug stability and malignant tumor traits. Targeting SIRT2 may be a way to treat basal-like breast cancer in humans if further research confirm these findings.