Affiliation:
1. Department of Breast Surgery, The Second Hospital of Shanxi Medical University, Taiyuan Shanxi 030001, China
2. The Second Group of Geriatrics Department, The Second Hospital of Shanxi Medical University, Taiyuan Shanxi 030001, China
3. Clinical Laboratory, The Second Hospital of Shanxi Medical University, Taiyuan Shanxi 030001, China
4. Department of Breast Surgery, Shanxi Bethune Hospital, Taiyuan Shanxi 030032, China
Abstract
Breast cancer (BC), which is most commonly seen in women, has become the second most common cause of cancer death in the United States. The number of women dying from BC is increasing every year, especially in the developing countries that fall behind in terms of economy and technologies.
Therefore, it is of great necessity to find potential targets to effectively treat this disease. In this study, RT-qPCR was performed to detect the expressions of TCL6, miR-665, and CD82. CCK-8 and immunofluorescence assays were conducted for the assessment of BC cell proliferation. The invasion
and migration of BC cells were detected by transwell and wound healing assays, respectively. Luciferase reporter assay was used to verify the combination of TCL6 and miR-665, and the binding of miR-665 and CD82. Moreover, the proliferation and migration of related proteins were measured by
western blot. The results showed that TCL6 was low expressed in BC cells, but overexpression of TCL6 inhibited the proliferation, migration, and invasion of BC cells. On the contrary, miR-665 was highly expressed in BC cells, while its expression was negatively correlated with TCL6 as suggested
by RT-qPCR assay. Furthermore, the inhibitory effects of TCL6 overexpression on the proliferation, migration, and invasion of BC cells were reversed by miR-665 mimic. Afterwards, the binding sites between miR-665 and CD82 were verified by luciferase reporter assay. Overexpression of TCL6 increased
the level of CD82 in BC cells, but this effect was reversed by miR-665 mimic as well. In conclusion, the present study has presented the fact that TCL6 could enhance the expression of CD82 by down-regulating the expression of miR-665.
Publisher
American Scientific Publishers
Subject
Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology