Semaphorin signaling via MICAL3 induces symmetric cell division to expand breast cancer stem-like cells.
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Drugs that disrupt the proliferation of cancer stem-like cells (CSCs) in breast tumours could help eliminate disease and prevent recurrence. A newly discovered signalling pathway now offers several promising therapeutic targets against CSCs.
A Kanazawa University-led team identified a signalling molecule called semaphorin that induces the symmetric division of breast CSCs, a type of copying that makes the cancer more malignant and aggressive.
To counteract the division, the researchers experimentally knocked down the expression of other molecules that mediate semaphorin signalling in CSCs and saw that their tumour-initiating activity was markedly reduced after implantation into mice.
They also showed that patients with breast cancer tend to have poor outcomes if their tumour cells express high levels of a particular semaphorin-associated protein, indicating that the study findings — and the idea of targeting this pathway — could prove clinically relevant.
- PNAS 116, 625–630 (2019). doi: 10.1073/pnas.1806851116
|The University of Tokyo Hospital, Japan||0.31|
|The University of Tokyo (UTokyo), Japan||0.16|
|Kanazawa Medical University, Japan||0.10|
|Showa General Hospital, Japan||0.10|
|Kanazawa University (KU), Japan||0.09|
|National Cancer Center (NCC), Japan||0.06|
|Minami Machida Hospital, Japan||0.05|
|Osaka University, Japan||0.05|
|Osaka University Hospital, Osaka University, Japan||0.05|
|Kyushu University, Japan||0.05|