首页> 外文期刊>Cell biology international. >Involvement of interleukin-1β mediated nuclear factor κB signalling pathways to down-regulate prostate-specific antigen and cell proliferation in LNCaP prostate cancer cells.
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Involvement of interleukin-1β mediated nuclear factor κB signalling pathways to down-regulate prostate-specific antigen and cell proliferation in LNCaP prostate cancer cells.

机译:白介素-1β介导的核因子κB信号通路参与下调LNCaP前列腺癌细胞的前列腺特异性抗原和细胞增殖。

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摘要

Involvement of NF-κB (nuclear factor κB) mediated by IL-1β (interleukin-1β) on cell proliferation and PSA (prostate-specific antigen) production of LNCaP prostate cell lines and the possible cross-talk with Akt (also known as protein kinase B) signalling pathway has been investigated. NF-κB and Akt were analysed by Western blotting from LNCaP cells treated by IL-1β before proliferation and PSA production were measured. IL-1β inhibited proliferation and decreased PSA production. The Akt pathway was not sensitive, whereas NF-κB phosphorylation occurred as a result of treatment. PSA production and proliferation of LNCaP cells were down-regulated by NF-κB mediated by IL-1β promoting anti-apoptotic signalling and co-suppressor factors of PSA expression. IL-1β through NF-κB activation provides a rationale for therapeutic approaches in the anticancer treatment of prostate.
机译:IL-1β(白介素-1β)介导的NF-κB(核因子κB)参与LNCaP前列腺细胞系的细胞增殖和PSA(前列腺特异性抗原)产生以及与Akt(也称为蛋白质)的串扰已经研究了激酶B)信号传导途径。在测量增殖和PSA产生之前,通过Western印迹分析IL-1β处理的LNCaP细胞的NF-κB和Akt。 IL-1β抑制增殖并降低PSA产生。 Akt途径不敏感,而NF-κB磷酸化是治疗的结果。 IL-1β介导的NF-κB促进PSA表达的抗凋亡信号和共抑制因子,下调LNCaP细胞的PSA产生和增殖。 IL-1β通过NF-κB的活化为前列腺癌的抗癌治疗提供了理论依据。

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