期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 24, 页码 -出版社
MDPI
DOI: 10.3390/ijms232416028
关键词
M-CSF; CSF-1 receptor; prostate; C2H cell line; TRAMP; osteopontin; SPP1; transcriptome
This study investigates the functionality of the CSF-1 receptor in prostate cancer cells and discovers that it can activate multiple signaling pathways and promote cell growth and invasion. They also find that activation of the CSF-1 receptor increases the expression of osteopontin, a key player in cancer development and metastasis. Therefore, the CSF-1 receptor may be a potential therapeutic target for the treatment of prostate cancer.
Prostate cancer is a major public health concern and one of the most prevalent forms of cancer worldwide. The definition of altered signaling pathways implicated in this complex disease is thus essential. In this context, abnormal expression of the receptor of Macrophage Colony-Stimulating Factor-1 (M-CSF or CSF-1) has been described in prostate cancer cells. Yet, outcomes of this expression remain unknown. Using mouse and human prostate cancer cell lines, this study has investigated the functionality of the wild-type CSF-1 receptor in prostate tumor cells and identified molecular mechanisms underlying its ligand-induced activation. Here, we showed that upon CSF-1 binding, the receptor autophosphorylates and activates multiple signaling pathways in prostate tumor cells. Biological experiments demonstrated that the CSF-1R/CSF-1 axis conferred significant advantages in cell growth and cell invasion in vitro. Mouse xenograft experiments showed that CSF-1R expression promoted the aggressiveness of prostate tumor cells. In particular, we demonstrated that the ligand-activated CSF-1R increased the expression of spp1 transcript encoding for osteopontin, a key player in cancer development and metastasis. Therefore, this study highlights that the CSF-1 receptor is fully functional in a prostate cancer cell and may be a potential therapeutic target for the treatment of prostate cancer.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据