| Literature DB >> 27829549 |
Liang Peng1, Zhigang Song1, Demeng Chen2, Ruixia Linghu1, Yingzhe Wang1, Xingyang Zhang1, Xiaoxue Kou1, Junlan Yang3, Shunchang Jiao4.
Abstract
GINS2, a subunit of GINS complex, is critical for the initiation of DNA replication and DNA replication fork progression. The expression of GINS2 is misregulated in many malignant tumors, such as leukemia, breast cancer and melanoma. However, the role of GINS in breast cancer remains poorly characterized. We investigate the possible effect and particular mechanism of GINS in breast cancer cells. We showed that expression of GINS2 is enriched in triple negative breast cancer (TNBC) cell lines. Furthermore, GINS2 knockdown decreased the growth, invasive ability and stem-like property of TNBC cells. Mechanistically, silencing of GINS2 in TNBC cells caused dramatic decrease of matrix metalloproteinase-9 (MMP9). Finally, the abundance of GINS2 correlated with the advance stages of tumor in human TNBC patients. Our studies provided insight into the molecular regulation of TNBC progression and invasion. More importantly, our data suggest that GINS2 could be an outstanding therapeutic target for inhibiting invasive TNBC growth and metastasis.Entities:
Keywords: Cancer stem cells; GINS; GINS2; MMP9; Triple negative breast cancer
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Year: 2016 PMID: 27829549 DOI: 10.1016/j.biopha.2016.10.032
Source DB: PubMed Journal: Biomed Pharmacother ISSN: 0753-3322 Impact factor: 6.529