LMO2 promotes tumor cell invasion and metastasis in basal-type breast cancer by altering actin cytoskeleton remodeling
Metrics: PDF 1776 views | HTML 2260 views | ?
Ye Liu1, Zhaoyang Wang1, Di Huang1, Chao Wu1, Huihui Li1, Xin Zhang2, Bin Meng3, Zongjin Li4, Tianhui Zhu1, Shuang Yang1, Wei Sun1
1Laboratory of Molecular Genetics in School of Medicine, Nankai University, Tianjin, China
2Department of Histology and Embryology in School of Medicine, Nankai University, Tianjin, China
3Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China
4Laboratory of Stem cells in School of Medicine, Nankai University, Tianjin, China
Wei Sun, email: firstname.lastname@example.org
Shuang Yang, email: email@example.com
Keywords: LMO2, actin filament, basal-type breast cancer, metastasis, cofilin1
Received: April 20, 2016 Accepted: November 02, 2016 Published: November 17, 2016
LMO2 is traditionally recognized as a pivotal transcriptional regulator during embryonic hematopoiesis and angionenesis, and its ectopic expression in T lymphocyte progenitors is closely correlated to the onset of acute T lymphocytic leukemia. However, recently studies revealed complicated expression features and dual functions of LMO2 on tumor behaviors in a variety of cancer types, including breast cancers. Basal-type breast cancer is one of the breast cancer subtypes and a prognostically unfavorable subtype among all breast cancers. Herein we found that in basal-type breast cancer specifically, high LMO2 expression was positively correlated with lymph node metastases in patients, promoted tumor cell migration and invasion and increased distant metastasis in SCID mice. Moreover, the novel function of LMO2 was achieved by its predominantly cytoplasmic location and interaction with cofilin1, which is a critical regulator in actin cytoskeleton dynamics. These findings suggest a subtype-dependent role of LMO2 in breast cancers and the potential of LMO2 as a subtype-specific biomarker for clinical practice.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.