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The role of NUMB/NUMB isoforms in Cancer Stem and Stem Cells
Hye Yeon Choi1 (Research associate), Jaekwon Seok 1 (ph.D student), Geun-Ho Kang 1 (ph.D student), Kyung Min Lim 1 (ph.D student), Ssang-Goo Cho 1,* (Professor)
1 Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California (90033), USA,
2Department of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Konkuk University, 120 Neungdong-ro Gwangjin-gu, Seoul 05029, Republic of Korea
Abstract
Cancer stem cells (CSCs) are a subpopulation of cancer that can self-renew and differentiate into large tumor masses. Evidence accumulated in recent years is that CSCs affect tumor proliferation, recurrence, and resistance to chemotherapy. Recent studies have shown that, like stem cells, CSCs maintain cells with self-renewal capacity by means of asymmetric division and promote cell proliferation by means of symmetric division. This cell division is regulated by fate determinants, such as the NUMB protein, which recently has also been confirmed as a cancer suppressor. Loss of NUMB expression leads to uncontrolled proliferation and amplification of the CSC pool, which promotes the Notch signaling pathway and reduces the expression of the p53 protein. NUMB genes are alternatively spliced to produce six functionally distinct isoforms. An interesting recent discovery is that the protein NUMB isoform produced by alternative splicing of NUMB plays an important role in promoting carcinogenesis. In this review, we summarize the known functions of NUMB and NUMB isoforms related to the proliferation and generation of CSCs.
Abstract, Accepted Manuscript(in press) [Submitted on April 6, 2021, Accepted on May 17, 2021]
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