Potential role of CXCR3 in proliferation and invasion of prostate cancer cells
To investigate the potential role of CXCR3 expression on prostate cancer cell proliferation and invasion and to illustrate its mechanism. Human PC-3 cells were transfected with siRNA-CXCR3A and siRNA-CXCR3B plasmids respectively. The mRNA expressions of CXCR3A and CXCR3B in PC-3 cells from each grou...
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Published in | International journal of clinical and experimental pathology Vol. 8; no. 7; pp. 8091 - 8098 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
e-Century Publishing Corporation
01.01.2015
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Subjects | |
Online Access | Get full text |
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Summary: | To investigate the potential role of CXCR3 expression on prostate cancer cell proliferation and invasion and to illustrate its mechanism.
Human PC-3 cells were transfected with siRNA-CXCR3A and siRNA-CXCR3B plasmids respectively. The mRNA expressions of CXCR3A and CXCR3B in PC-3 cells from each group were analyzed using RT-PCR. Besides, cell proliferation ability and cell invasion ability of PC-3 cells in each group were analyzed using MTT assay and Matrige assay respectively. Additionally, expressions of CXCR3 downstream proteins were detected using Western blotting.
mRNA level of CXCR3A was decreased while CXCR3B mRNA level was increased in PC-3 cells (P<0.05). Compared with the controls, down-regulation of CXCR3A but up-regulation of CXCR3B significantly inhibited PC-3 cell proliferation and cell invasion ability (P<0.05). Besides, aberrant CXCR3 expression significantly increased expressions of phospholipase C (PLCβ), matrix metallo proteinase (MMP-1), and MMP-3 except MMP-7 in PC-3 cells (P<0.05).
The data presented in our study suggested that aberrant CXCR3 expression may play crucial roles in suppressing PC metastasis via inhibiting cell proliferation and invasion ability through the PCLβ signaling pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Co-first authors. |
ISSN: | 1936-2625 |