scholarly journals Arsenic trioxide inhibits viability and induces apoptosis through reactivating the Wnt inhibitor secreted frizzled related protein-1 in prostate cancer cells

2016 ◽  
pp. 885 ◽  
Author(s):  
Tao Jiang ◽  
Lei Zheng ◽  
Hui Jiang ◽  
Zhi-Wei Zhang ◽  
Ke-nan Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Related Protein ◽  
Prostate Cancer Cells ◽  
Wnt Inhibitor

AS1 expression in prostate cancer and its effects on proliferation and invasion of prostate cancer cells

2021 ◽  
pp. 1-9
Author(s):  
Yuxin Li ◽  
Xiaohong Zhuang ◽  
Li Zhuang ◽  
Hongjian Liu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Related Protein ◽  
Prostate Cancer Cells ◽  
Blank Group ◽  
Normal Prostate ◽  
Cell Cycles ◽  
Prostate Cells ◽  
Proliferation And Invasion

This paper aimed at investigating AS1 expression in prostate cancer (PCa) and its effects on the proliferation and invasion of prostate cancer cells (PCCs). The prostate tissues and the matched adjacent normal prostate tissues excised and preserved during radical prostatectomy in our hospital were collected. The LncRNA NCK1-AS1 expression was detected. PCa patients were followed up for three years to analyze their prognosis. The correlation of LncRNA NCK1-AS1 expression with clinicopathological features was analyzed. Human normal prostate cells and human PCCs were selected, in which LncRNA NCK1-AS1 expression was tested to screen and then transfect the cells. Cell proliferation, invasion and migration were detected. Cell cycles and apoptosis were analyzed. Compared with the adjacent normal tissues, LncRNA NCK1-AS1 was highly expressed in the prostate cancer tissues. Its expression was remarkably different in those with different stages of TNM and with lymphatic metastasis or not. The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression. Compared with the human normal prostate cells, LncRNA NCK1-AS1 expression in the human PCCs remarkably rose, with the greatest difference in 22Rv1 cells. Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group. Additionally, in this group, the number of invasive and migratory cells remarkably reduced; the expression of invasion-related protein E-cadherin remarkably rose but that of MMP-2 remarkably reduced; cell cycles were arrested and the expression of cycle-related proteins (CDK4, CDK6, cyclin D1) remarkably reduced; the apoptotic rate and the expression of apoptosis-related protein Bax remarkably rose. LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.

scholarly journals Combination of Arsenic trioxide and Everolimus (Rad001) synergistically induces both autophagy and apoptosis in prostate cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (7) ◽  
pp. 11206-11218 ◽  
Author(s):  
Sheng Tai ◽  
Lingfan Xu ◽  
Ming Xu ◽  
Ligang Zhang ◽  
Yangyang Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Prostate Cancer Cells

Abstract 1109: Characterization of hepatoma-derived growth factor (HDGF) as a novel survival related protein in prostate cancer cells

2011 ◽  
Author(s):  
Gnanasekar Munirathinam ◽  
Aditya Shetty ◽  
Abhilash Samykutty ◽  
Gajalakshmi Dakshinamoorthy ◽  
Guoxing Zheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Related Protein ◽  
Prostate Cancer Cells

Novel combination therapy of prostate cancer cells with arsenic trioxide and flutamide: An in-vitro study

2022 ◽  
Vol 74 ◽  
pp. 101684
Author(s):  
Akram Mirzaei ◽  
Mohammad Reza Akbari ◽  
Seyed Saeed Tamehri Zadeh ◽  
Fatemeh Khatami ◽  
Rahil Mashhadi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
In Vitro Study ◽  
Vitro Study ◽  
Prostate Cancer Cells

scholarly journals AICAR induces apoptosis and inhibits migration of prostate cancer cells through an AMPK/mTOR-dependent pathway

2018 ◽  
Author(s):  
Chia-Cheng Su ◽  
Kun-Lin Hsieh ◽  
Shu-Chi Wang ◽  
Hsin-Chih Yeh ◽  
Shu-Pin Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cell Growth ◽  
Western Blot ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Parp Cleavage ◽  
Related Protein ◽  
Prostate Cancer Cells ◽  
Dependent Pathway

AbstractAICAR (5-aminoimidazole-4-carbox-amide-1-β-D-ribofuranoside), an AMP-activated protein kinase (AMPK) agonist, has demonstrated antitumor activities for several types of cancers. However, the activity of AICAR on the cell growth and metastasis of prostate cancer has not been extensively studied. Herein we examine the effects of AICAR on the cell growth and metastasis of prostate cancer cells, 22RV1 cells. Cell growth was performed by MTT assay and soft agar assay. Cell apoptosis was examined by Annexin V/PI staining and PARP cleavage Western blot. Cell migration was evaluated by wound-healing assay. The expression of EMT-related protein and the activity of the AMPK/ mTOR-dependent pathway were analyzed by Western blot. In addition, we also tested the effect of AICAR on the chemosensitivity to docetaxel using MTT assay. Our results indicated that AICAR inhibits cell growth, induces apoptosis, attenuates TGF-β-induced cell migration and EMT-related protein expression, and enhances the chemosensitivity to docetaxel through regulating the AMPK/mTOR-dependent pathway. Collectively, these findings support AICAR as a potential therapeutic agent for the treatment of prostate cancer.

Sign in / Sign up

Export Citation Format

Share Document