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Growth hormone receptor promotes breast cancer progression via the BRAF/MEK/ERK signaling pathway.
FEBS Open Bio ( IF 2.8 ) Pub Date : 2020-05-06 , DOI: 10.1002/2211-5463.12816
Xiaojue Zhu 1 , Yonghao Li 1 , Guoxin Xu 1 , ChangQing Fu 2
Affiliation  

Growth hormone receptor (GHR), a member of the class I cytokine receptor family, plays key roles in cancer progression. Recently, GHR has been reported to be associated with breast cancer development, but the molecular mechanism of GHR in this malignancy is not fully understood. To investigate this issue, we stably inhibited GHR in breast cancer cell lines, which were observed to reduce cell proliferation, tumor growth and induction of apoptosis, and arrest the cell‐cycle arrest at the G1–S phase transition. In addition, GHR silencing suppressed the protein levels of B‐Raf proto‐oncogene, serine/threonine kinase (BRAF), Mitogen‐activated protein kinase kinase (MEK) and Extracellular regulated protein kinases (ERK). These findings suggest that GHR may mediate breast cell progression and apoptosis through control of the cell cycle via the BRAF/MEK/ERK signaling pathway.

中文翻译:

生长激素受体通过BRAF / MEK / ERK信号通路促进乳腺癌的进展。

生长激素受体(GHR)是I类细胞因子受体家族的成员,在癌症进展中起关键作用。最近,据报道GHR与乳腺癌的发展有关,但是GHR在这种恶性肿瘤中的分子机制尚不完全清楚。为了研究这个问题,我们稳定地抑制了乳腺癌细胞株中的GHR,观察到它们可减少细胞增殖,肿瘤生长和凋亡诱导,并在G1-S相变中阻止细胞周期停滞。此外,GHR沉默抑制了B-Raf原癌基因,丝氨酸/苏氨酸激酶(BRAF),丝裂原激活的蛋白激酶激酶(MEK)和细胞外调节蛋白激酶(ERK)的蛋白质水平。
更新日期:2020-05-06
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