AsianScientist (Feb. 1, 2019) – Cancer stem cells (CSCs) are one of the reasons cancer recurs in patients. In a study published in the Proceedings of the National Academy of Sciences, scientists in Japan have discovered a mechanism by which CSCs form and multiply in breast cancer.
Breast cancer is one of the most common cancers in women and breast tumors contain a small population of CSCs which are not targeted by conventional treatments such as chemotherapy or radiotherapy followed by oral drug administration. Developing novel treatments to destroy CSCs is challenging as researchers do not fully understand how CSCs come about.
In this study, scientists led by Professor Noriko Gotoh from Kanazawa University, Japan, have uncovered a signaling pathway directly related to the proliferation of CSCs in breast cancer. They reported that breast CSCs largely take the path of symmetric division, where two self-renewing CSCs are formed after cell division.
Delving into the mechanism by which symmetric division of breast CSCs occur, the team noticed that a gene encoding a protein known as Semaphorin 3 (Sema3) was highly expressed in the microenvironment of CSCs. The production of Sema3 activates another protein, called MICAL3. Together, Sema3 and MICAL3 triggered a series of biomolecular interactions that led to the symmetric division of CSCs. The team further noted that elevated levels of Sema3 and MICAL3 were required for tumor sphere formation.
Gotoh and colleagues suggest that the number of CSCs in breast cancer can be controlled by inhibition of MICAL3 or by genetically silencing the signaling pathway triggered by Sema3. Their findings could lead to better treatments for breast cancer and lower the incidence of breast cancer recurrence.
The article can be found at: Tominaga et al. (2018) Semaphorin Signaling via MICAL3 Induces Symmetric Cell Division to Expand Breast Cancer Stem-like Cells.
Source: Kanazawa University; Photo: Shutterstock.
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