RUNX1 as a Novel Molecular Target for Breast Cancer

被引:8
|
作者
Ariffin, Nur Syamimi [1 ,2 ]
机构
[1] Univ Teknol MARA, Fac Pharm, Dept Pharmacol & Pharmaceut Chem, Selangor, Malaysia
[2] Univ Teknol MARA, Fac Pharm, Dept Pharmacol & Pharmaceut Chem, UiTM Selangor Branch, Puncak Alam Campus, Selangor 42300, Malaysia
关键词
RUNX1; Breast cancer; Oncogene; Tumor suppressor; Molecular target; TRANSCRIPTION FACTORS; STEM-CELLS; GENE; LEUKEMIA; EXPRESSION; TRANSLOCATIONS; HEMATOPOIESIS; CHEMOTHERAPY; ASSOCIATION; METASTASIS;
D O I
10.1016/j.clbc.2022.04.006
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
RUNX1 has long known for its role in hematopoiesis until recently it is implicated in human breast cancer pathogenesis. This has drawn attention in research as elevated expression of RUNX1 has been observed in invasive breast cancer, and mutations of the RUNX1 gene and its binding partner CBF beta have been identified in luminal breast cancer patients, many of which have attributed to the development and progression of the disease. Increasing number of evidence also shows the involvement of RUNX1 in breast cancer migration and invasion that may lead to breast cancer metastasis. However, more studies need to be conducted to better understand its roles in these particular subtypes in breast cancer. This is important as evidence so far indicates that there are discrepancies with regards to the roles of RUNX1 in ER-positive and ER-negative breast cancer, both of which have posted a great challenge to recognize whether its deregulation is protecting or promoting breast cancer. This warrants further analysis to glean more information especially considering the perturbation of RUNX1 is mainly reported in ER-positive breast cancer. In this review, the roles of RUNX1 in breast cancer are discussed in a context dependent manner based on its involvement in the development and progression of the disease. The association of RUNX1 with other types of cancer is also included to emphasize a wider and possibly a different angle of involvement of RUNX1 in cancer.
引用
收藏
页码:499 / 506
页数:8
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