The FTO m6A demethylase inhibits the invasion and migration of prostate cancer cells by regulating total m6A levels

Life Sciences ◽  
2021 ◽  
Vol 271 ◽  
pp. 119180
Author(s):  
Kai Zhu ◽  
Ying Li ◽  
Yikai Xu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Silencing of BACH1 inhibits invasion and migration of prostate cancer cells by altering metastasis-related gene expression

2017 ◽  
Vol 46 (7) ◽  
pp. 1495-1504 ◽  
Author(s):  
Neda Shajari ◽  
Sadaf Davudian ◽  
Tohid Kazemi ◽  
Behzad Mansoori ◽  
Shima Salehi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Related Gene ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells

Tumor Biology ◽  
2016 ◽  
Vol 37 (12) ◽  
pp. 16163-16176 ◽  
Author(s):  
Jin-Hua He ◽  
Bao-Xia Li ◽  
Ze-Ping Han ◽  
Mao-Xian Zou ◽  
Li Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

scholarly journals Inhibition of invasion and migration of prostate cancer cells by miRNA-509-5p via targeting MDM2

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
X.M. Tian ◽  
Y.Z. Luo ◽  
P. He ◽  
J. Li ◽  
Z.W. Ma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals MicroRNA‑155‑5p inhibits the invasion and migration of prostate cancer cells by targeting SPOCK1

2020 ◽  
Vol 20 (6) ◽  
pp. 1-1
Author(s):  
Lin-Ya Yao ◽  
Jun Ma ◽  
Xue-Ming Zeng ◽  
Jun Ou‑yang
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Human bone marrow mesenchymal stem cells-derived microRNA-205-containing exosomes impede the progression of prostate cancer through suppression of RHPN2

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Shuangjian Jiang ◽  
Chengqiang Mo ◽  
Shengjie Guo ◽  
Jintao Zhuang ◽  
Bin Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Human bone marrow mesenchymal stem cells (hBMSCs) are implicated in cancer initiation and metastasis, sometimes by releasing exosomes that mediate cell communication by delivering microRNAs (miRNAs). This study aimed to investigate the physiological mechanisms by which exosomal miR-205 derived from hBMSCs may modulate the growth of prostate cancer cells. Methods Microarray-based gene expression profiling of prostate cancer was adopted to identify differentially expressed genes and regulatory miRNAs, which identified the candidates RHPN2 and miR-205 as the study focus. Then the binding affinity between miR-205 and RHPN2 was identified using in silico analysis and luciferase activity detection. Prostate cancer cells were co-cultured with exosomes derived from hBMSCs treated with either miR-205 mimic or miR-205 inhibitor. Subsequently, prostate cancer cell proliferation, invasion, migration, and apoptosis were detected in vitro. The effects of hBMSCs-miR-205 on tumor growth were investigated in vivo. Results miR-205 was downregulated, while RHPN2 was upregulated in prostate cancer cells. RHPN2 was a target of miR-205, and upregulated miR-205 inhibited prostate cancer cell proliferation, invasion, and migration and promoted apoptosis by targeting RHPN2. Next, experiments demonstrated that hBMSCs-derived exosomes carrying miR-205 contributed to repressed prostate cancer cell proliferation, invasion, and migration and enhanced apoptosis. Furthermore, in vivo assays confirmed the inhibitory effects of hBMSCs-derived exosomal miR-205 on prostate cancer. Conclusion The hBMSCs-derived exosomal miR-205 retards prostate cancer progression by inhibiting RHPN2, suggesting that miR-205 may present a predictor and potential therapeutic target for prostate cancer.

scholarly journals Estrogen Receptor α Is Crucial in Zearalenone-Induced Invasion and Migration of Prostate Cancer Cells

Toxins ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 98 ◽  
Author(s):  
Karolina Kowalska ◽  
Dominika Habrowska-Górczyńska ◽  
Kinga Urbanek ◽  
Kamila Domińska ◽  
Agnieszka Piastowska-Ciesielska
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Α ◽  
Prostate Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells

2015 ◽  
Vol 36 (2) ◽  
pp. 799-809 ◽  
Author(s):  
Qingfeng Hu ◽  
Shijun Tong ◽  
Xiaojun Zhao ◽  
Weihong Ding ◽  
Yuancheng Gou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Associated Factors ◽  
Epithelial Mesenchymal Transition ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Background: In our previous study, we found that periostin was upregulated in prostate cancer, and its expression could be modulated by TGF-β. TGF-β could upregulate periostin expression in some cells, and both TGF-β and periostin could induce epithelial mesenchymal transition (EMT). We aimed to study the effect of periostin in the process of TGF-β-induced EMT in prostate cancer cells. Methods: We constructed a lentivirus vector containing the periostin gene and transduced it into PC3 and DU145 cells. After confirming periostin overexpression by PCR and Western blotting, we used an MTT assay to establish a growth curve to measure cell proliferation. Additionally, we performed transwell and wound healing assays to measure cell invasion and migration, respectively. Lastly, we measured the expression of EMT associated factors using Western blot analysis to test the effect of periostin on EMT in prostate cancer cells. Results: PCR and Western blot analyses confirmed that periostin was upregulated after infection with the periostin lentiviral vector. Periostin overexpression promoted increased cell proliferation, invasion, and migration as measured by MTT, transwell, and wound healing assays, respectively. Western blot analysis illustrated that periostin overexpression increased the expression of EMT associated factors, and periostin overexpression activated Akt and GSK-3β, which could be inhibited using a PI3K inhibitor. Additionally, TGF-β increased the levels of STAT3, Twist1 and periostin, while both STAT3 shRNA and Twist1 shRNA inhibited periostin expression. However, STAT3 shRNA also decreased Twist1 expression. Although reduction of STAT3, Twist1 or periostin levels with shRNA inhibited TGF-β-induced overexpression of EMT associated factors, periostin overexpression could reverse such inhibition by interfering with STAT3 and Twist1. Similarly, periostin overexpression also reversed inhibition of cell invasion induced by interference of STAT3 and Twist1. Conclusion: Our findings indicate that periostin is an important mediator of TGF-β-induced EMT and suggest that periostin is a potential therapeutic target for suppressing the metastatic progression of prostate cancer.

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