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Abstract
Breast cancer (BC) is one of the primary tumors with high incidence in women. The
purpose of this study was to investigate the role of LINC00473 and underlying mechanisms
in BC. Expression pattern of LINC00473 was analyzed using qRT-PCR (quantitative real-time
polymerase chain reaction) assays in BC tissues and cells. Overexpression or knockdown
of LINC00473 in vitro and functional experiments were performed to study its effects
on BC cells. Target prediction, luciferase assays, RNA fluorescence in situ hybridization
and RNA immunoprecipitation were used to verify the role of LINC00473 as a competing
endogenous RNA. The impact of LINC00473 on tumor growth was also evaluated using a
xenograft model. In our study, we found that LINC00473 was highly expressed in BC
tissues and cells, and the elevated expression was correlated with shorter overall
survival in patients with BC. Furthermore, knockdown of LINC00473 significantly inhibited
the capacity of proliferation, invasion and migration of BC cells. Animal experiment
suggested that silencing LINC00473 could significantly inhibit the tumor growth. Following
experiments revealed that LINC00473 may function as a competing endogenous RNA to
regulate the expression of Mitogen-Activated Protein Kinase 1 (MAPK1) through competition
for miR-198. Thus, increased expression of LINC00473 in breast cancer tissues is linked
to poor prognosis. LINC00473 may function as an endogenous completive RNA by sponging
miR-198 to regulate MAPK1 expression. Findings of our study contributed to the basis
for further exploring the application of LINC00473 as a prognostic and diagnostic
biomarker.