IGHG1 Regulates Prostate Cancer Growth via the MEK/ERK/c-Myc Pathway
IGHG1 Regulates Prostate Cancer Growth via the MEK/ERK/c-Myc Pathway
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DOI：
10.1155/2019/7201562
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发表时间：
2019-01-01
影响因子：
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通讯作者：
Pan, Bin
中科院分区：
文献类型：
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作者：
Chu, Jing;Li, Yutong;Pan, Bin
越来越多的证据表明，免疫球蛋白是重要的各种癌症，包括前列腺癌（PCa）的调节。然而，IgG调节PCa发展的潜在机制仍有待进一步探讨。在这里，我们证明了IgG 1重链（IGHG 1）在PCa患者的组织中增加。通过抗体阻断或基因敲低抑制IGHG 1抑制细胞生长并诱导细胞周期停滞和最终凋亡。c-Myc表达水平与IGHG 1水平呈正相关。在体外培养的前列腺癌细胞中，MEK/ERK/c-Myc信号通路位于IGHG 1的下游。抑制IGHG 1可抑制裸鼠移植瘤的生长，并在体内外阻断MEK/ERK/c-Myc信号通路。这些发现表明IGHG 1在前列腺癌的发展过程中起着至关重要的作用，抑制IGHG 1可能是治疗PCa的潜在疗法。
Increasing evidence indicates that immunoglobulins are important for the regulation of various cancers including prostate cancer (PCa). However, the underlying mechanisms of IgG regulated PCa development remain to be further explored. Here, we demonstrated that IgG1 heavy chain (IGHG1) was increased in tissues from PCa patients. Inhibition of IGHG1 by antibody blocking or genetic knockdown suppressed cell growth and induced cell cycle arrest and ultimate apoptosis. Expression levels of c-Myc were positively correlated with the levels of IGHG1. Furthermore, MEK/ERK/c-Myc pathway lied downstream of IGHG1 in cultured prostate cancer cells. Inhibition of IGHG1 restrained the tumor growth in nude mice and inactivated MEK/ERK/c-Myc pathway both in vitro and in vivo. These findings suggest that IGHG1 play a crucial role during the development of prostate cancer and inhibition of IGHG1 may be a potential therapy in the treatment of PCa.