Phosphorylation of LIFR promotes prostate cancer progression by activating the AKT pathway
Phosphorylation of LIFR promotes prostate cancer progression by activating the AKT pathway
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LIFR 磷酸化通过激活 AKT 通路促进前列腺癌进展
DOI：
10.1016/j.canlet.2019.02.042
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发表时间：
2019-01-01
期刊：
影响因子：
9.7
通讯作者：
Wang, Xiongjun
中科院分区：
文献类型：
--
作者：
Shao, Jialiang;Zhu, Wencheng;Wang, Xiongjun
前列腺癌（PCa）是男性中最常见的实体器官恶性肿瘤，数量超过肺癌和结直肠癌，并且由于高转移性，它是美国男性肿瘤相关死亡的第二大原因。最近，人们发现白血病抑制因子受体（LIFR）在多种类型的癌症中发挥作用。然而，LIFR 在 PCa 进展中的作用仍有待揭示。在这项研究中，我们发现 LIFR 在 PCa 中发挥致癌作用。 LIFR 在 51044 位点的磷酸化有助于随后激活 AKT 通路，诱导一系列增殖和转移基因的表达。另外，LIFR-S1044 被 ERK2 磷酸化，但 EFtK1 不磷酸化。 PCa 组织中 pLIFR-S1044 和 pAKT 5473 的信号强度显示出紧密的正相关性。 ERK2/LIFR/AKT 轴调节 PCa 进展，并为 PCa 提供有前途的治疗和诊断靶点。
Prostate cancer (PCa) is the most common solid organ malignancy among men, outnumbering both lung and colorectal cancer, and it is the second leading cause of male tumor-related death in the United States due to high metastasis. Recently, leukemia inhibitory factor receptor (LIFR) has been found to play roles in multiple types of cancer. However, the roles of LIFR in the progression of PCa remain to be revealed. In this study, we found that LIFR plays an oncogenic role in PCa. The phosphorylation of LIFR at 51044 contributes to subsequent activation of the AKT pathway, inducing the expression of a series of proliferation and metastatic genes. Additionally, LIFR-S1044 is phosphorylated by ERK2 but not EFtKl. The signal intensity of pLIFR-S1044 and pAKT 5473 in PCa tissue displays a tight positive correlation. The ERK2/LIFR/AKT axis modulates PCa progression and offers a promising therapeutic and diagnostic target for PCa.