Prostate cancer downregulated SIRP-α modulates apoptosis and proliferation through p38-MAPK/NF-κB/COX-2 signaling
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Prostate cancer downregulated SIRP-α modulates apoptosis and proliferation through p38-MAPK/NF-κB/COX-2 signaling. / Yao, Chen; Li, Gang; Cai, Ming; Qian, Yeyong; Wang, Liqin; Xiao, Li; Thaiss, Friedrich; Shi, Bingyi.
In: ONCOL LETT, Vol. 13, No. 6, 06.2017, p. 4995-5001.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Prostate cancer downregulated SIRP-α modulates apoptosis and proliferation through p38-MAPK/NF-κB/COX-2 signaling
AU - Yao, Chen
AU - Li, Gang
AU - Cai, Ming
AU - Qian, Yeyong
AU - Wang, Liqin
AU - Xiao, Li
AU - Thaiss, Friedrich
AU - Shi, Bingyi
PY - 2017/6
Y1 - 2017/6
N2 - The present study investigated the regulatory mechanism of signal-regulatory protein (SIRP)-α in the apoptosis and proliferation of prostate cancer (CaP) cells. The expression profile of SIRP-α in prostate cancer cells was analyzed using reverse transcription-quantitative polymerase chain reaction and western blotting. Then SIRP-α function in CaP cells was further analyzed with the overexpression and RNA interference of SIRP-α. The results revealed that SIRP-α expression levels were decreased in CaP tissues and cell lines, with androgen-independent CaP exhibiting a lower SIRP-α expression compared with androgen-dependent CaP. Overexpression of SIRP-α resulted in a significantly reduced number of live CaP cells by enhancing apoptosis, whereas SIRP-α silencing increased CaP cell proliferation. Mechanistically, SIRP-α decreases cyclooxygenase-2 (COX-2) expression and cytokine production by negatively regulating p38 mitogen-activated protein kinase and nuclear factor-κB pathway. Therefore, SIRP-α knockdown decreases cell apoptosis by enhancing COX-2 expression. The present results indicate that SIRP-α may function as a novel negative regulator to modulate cellular proliferation, survival and migration in CaP cells. The heightened sensitivity of cells restoring SIRP-α function could be exploited in the development of therapeutics that may potentiate the antineoplastic effects of conventional cytokines or chemotherapeutic agents.
AB - The present study investigated the regulatory mechanism of signal-regulatory protein (SIRP)-α in the apoptosis and proliferation of prostate cancer (CaP) cells. The expression profile of SIRP-α in prostate cancer cells was analyzed using reverse transcription-quantitative polymerase chain reaction and western blotting. Then SIRP-α function in CaP cells was further analyzed with the overexpression and RNA interference of SIRP-α. The results revealed that SIRP-α expression levels were decreased in CaP tissues and cell lines, with androgen-independent CaP exhibiting a lower SIRP-α expression compared with androgen-dependent CaP. Overexpression of SIRP-α resulted in a significantly reduced number of live CaP cells by enhancing apoptosis, whereas SIRP-α silencing increased CaP cell proliferation. Mechanistically, SIRP-α decreases cyclooxygenase-2 (COX-2) expression and cytokine production by negatively regulating p38 mitogen-activated protein kinase and nuclear factor-κB pathway. Therefore, SIRP-α knockdown decreases cell apoptosis by enhancing COX-2 expression. The present results indicate that SIRP-α may function as a novel negative regulator to modulate cellular proliferation, survival and migration in CaP cells. The heightened sensitivity of cells restoring SIRP-α function could be exploited in the development of therapeutics that may potentiate the antineoplastic effects of conventional cytokines or chemotherapeutic agents.
KW - Journal Article
U2 - 10.3892/ol.2017.6070
DO - 10.3892/ol.2017.6070
M3 - SCORING: Journal article
C2 - 28588738
VL - 13
SP - 4995
EP - 5001
JO - ONCOL LETT
JF - ONCOL LETT
SN - 1792-1074
IS - 6
ER -