Androgen receptor-regulated miRNA-193a-3p targets AJUBA to promote prostate cancer cell migration

The Prostate ◽  
2017 ◽  
Vol 77 (9) ◽  
pp. 1000-1011 ◽  
Author(s):  
Li Jia ◽  
Bin Gui ◽  
Dali Zheng ◽  
Keith F. Decker ◽  
Ilker Tinay ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Migration

scholarly journals Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells

2019 ◽  
Vol 8 (3) ◽  
pp. 354 ◽  
Author(s):  
Kouji Izumi ◽  
Atsushi Mizokami
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Prostate Cancer Cell ◽  
Standard Form ◽  
Cancer Cell Migration ◽  
Prostate Cancer Cells

Androgen/androgen receptor (AR) signaling is a significant driver of prostate cancer progression, therefore androgen-deprivation therapy (ADT) is often used as a standard form of treatment for advanced and metastatic prostate cancer patients. However, after several years of ADT, prostate cancer progresses to castration-resistant prostate cancer (CRPC). Androgen/AR signaling is still considered an important factor for prostate cancer cell survival following CRPC progression, while recent studies have reported dichotomic roles for androgen/AR signaling. Androgen/AR signaling increases prostate cancer cell proliferation, while simultaneously inhibiting migration. As a result, ADT can induce prostate cancer metastasis. Several C-C motif ligand (CCL)-receptor (CCR) axes are involved in cancer cell migration related to blockade of androgen/AR signaling. The CCL2-CCR2 axis is negatively regulated by androgen/AR signaling, with the CCL22-CCR4 axis acting as a further downstream mediator, both of which promote prostate cancer cell migration. Furthermore, the CCL5-CCR5 axis inhibits androgen/AR signaling as an upstream mediator. CCL4 is involved in prostate carcinogenesis through macrophage AR signaling, while the CCL21-CCR7 axis in prostate cancer cells is activated by tumor necrotic factor, which is secreted when androgen/AR signaling is inhibited. Finally, the CCL2-CCR2 axis has recently been demonstrated to be a key contributor to cabazitaxel resistance in CRPC.

scholarly journals A novel long noncoding RNA LINC00844 regulates prostate cancer cell migration and invasion through androgen receptor signaling

2018 ◽  
Author(s):  
Shreyas Lingadahalli ◽  
Sudhir Jadhao ◽  
Ying Ying Sung ◽  
Mi Chen ◽  
Lingling Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Migration And Invasion ◽  
Metastasis Suppressor ◽  
Cancer Cell Migration ◽  
Normal Prostate ◽  
Cell Migration And Invasion

AbstractThe majority of the human genome is transcribed, yielding a rich repository of non-coding transcripts that are involved in a myriad of biological processes including cancer. However, how non-coding transcripts such as long non-coding RNAs (lncRNAs) function in prostate cancer is still unclear. In this study, we have identified a novel set of clinically relevant androgen-regulated lncRNAs in prostate cancer. Among this group, we showed LINC00844 is a direct androgen-regulated target that is actively transcribed in androgen receptor (AR)-dependent prostate cancer cells. The expression of LINC00844 is higher in normal prostate compared to malignant and metastatic prostate cancer samples and patients with low expression demonstrate poor prognosis and significantly increased biochemical recurrence, suggesting LINC00844 may function in suppressing tumor progression and metastasis. Indeed,in-vitroloss-of-function studies revealed that LINC00844 prevents prostate cancer cell migration and invasion. Moreover, findings from gene expression analysis indicated that LINC00844 functions intrans, affecting global androgen-regulated gene transcription. Mechanistically, we provide evidence to show LINC00844 is important in facilitating AR binding to the chromatin. Finally, we demonstrated LINC00844 mediates its phenotypic effects in part by activating the expression of NDRG1, a crucial cancer metastasis suppressor. Collectively, our findings suggest LINC00844 is a novel coregulator of AR that plays a central role in the androgen transcriptional network and the development and progression of prostate cancer.

scholarly journals Novel lncRNA LINC00844 Regulates Prostate Cancer Cell Migration and Invasion through AR Signaling

2018 ◽  
Vol 16 (12) ◽  
pp. 1865-1878 ◽  
Author(s):  
Shreyas Lingadahalli ◽  
Sudhir Jadhao ◽  
Ying Ying Sung ◽  
Mi Chen ◽  
Lingling Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion

A PAK4–LIMK1 pathway drives prostate cancer cell migration downstream of HGF

2008 ◽  
Vol 20 (7) ◽  
pp. 1320-1328 ◽  
Author(s):  
Tasneem Ahmed ◽  
Kerry Shea ◽  
John R.W. Masters ◽  
Gareth E. Jones ◽  
Claire M. Wells
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Migration
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