This week we profile a recent publication in Nature Communications from the laboratory
of Dr. Shoukat Dedhar at the BC Cancer Agency.
Can you provide a brief overview of your lab’s current research focus?
Cancer cells have been observed to frequently have amplified centrosomes. These amplified centrosomes must be actively clustered together for cancer cells to divide. Since normal cells do not have centrosome amplification, targeting centrosome clustering is a highly specific way to target cancer cells while sparing normal cells. We performed an automated screen for compounds that inhibited centrosome clustering and identified a Stat3 inhibitor. We are currently trying to characterize this pathway and translate this observation into a clinically-relevant data.
What is the significance of the findings in this publication?
We identified a novel Stat3-dependent pathway that cancer cells with amplified centrosomes rely on to divide. There are currently several clinical trials testing Stat3 inhibitors in cancer patients and a better understanding of Stat3 signalling is important for determining which patients will respond to Stat3 inhibitors and what drug combinations might be most effective.
Briefly, what are the next steps for this research?
The next step is to develop an assay to screen patient samples that have the centrosome amplifications we observed and then determine whether these cancer patients with centrosome amplification respond better to Stat3 inhibitors. We are also looking in other cancer types besides breast cancer to determine whether this pathway is a common feature in different cancers.
This project was supported by:
This work is funded by grants from the CIHR and CCSRI. We are grateful for their support.