scholarly journals URG11 Regulates Prostate Cancer Cell Proliferation, Migration, and Invasion

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Bin Pan ◽  
Yunlin Ye ◽  
Haiping Liu ◽  
Jianli Zhen ◽  
Hongmei Zhou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Colon Cancers

Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, is involved in the development and progression of several tumors, including liver, stomach, lung, and colon cancers. However, the role of URG11 in prostate cancer remains yet to be elucidated. By determined expression in human prostate cancer tissues, URG11 was found significantly upregulated and positively correlated with the severity of prostate cancer, compared with that in benign prostatic hyperplasia tissues. Further, the mRNA and protein levels of URG11 were significantly upregulated in human prostate cancer cell lines (DU145, PC3, and LNCaP), compared with human prostate epithelial cell line (RWPE-1). Moreover, by the application of siRNA against URG11, the proliferation, migration, and invasion of prostate cancer cells were markedly inhibited. Genetic knockdown of URG11 also induced cell cycle arrest at G1/S phase, induced apoptosis, and decreased the expression level of β-catenin in prostate cancer cells. Overexpression of URG11 promoted the expression of β-catenin, the growth, the migration, and invasion ability of prostate cancer cells. Taken together, this study reveals that URG11 is critical for the proliferation, migration, and invasion in prostate cancer cells, providing the evidence of URG11 to be a novel potential therapeutic target of prostate cancer.

scholarly journals Distinct roles for the RNA-binding protein Staufen1 in prostate cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kristen A. Marcellus ◽  
Tara E. Crawford Parks ◽  
Shekoufeh Almasi ◽  
Bernard J. Jasmin
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Rna Binding ◽  
Prostate Cancer Cell ◽  
Rna Binding Protein ◽  
Migration And Invasion ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Prostate Cells

Abstract Background Prostate cancer is one of the most common malignant cancers with the second highest global rate of mortality in men. During the early stages of disease progression, tumour growth is local and androgen-dependent. Despite treatment, a large percentage of patients develop androgen-independent prostate cancer, which often results in metastases, a leading cause of mortality in these patients. Our previous work on the RNA-binding protein Staufen1 demonstrated its novel role in cancer biology, and in particular rhabdomyosarcoma tumorigenesis. To build upon this work, we have focused on the role of Staufen1 in other forms of cancer and describe here the novel and differential roles of Staufen1 in prostate cancer. Methods Using a cell-based approach, three independent prostate cancer cell lines with different characteristics were used to evaluate the expression of Staufen1 in human prostate cancer relative to control prostate cells. The functional impact of Staufen1 on several key oncogenic features of prostate cancer cells including proliferation, apoptosis, migration and invasion were systematically investigated. Results We show that Staufen1 levels are increased in all human prostate cancer cells examined in comparison to normal prostate epithelial cells. Furthermore, Staufen1 differentially regulates growth, migration, and invasion in the various prostate cancer cells assessed. In LNCaP prostate cancer cells, Staufen1 regulates cell proliferation through mTOR activation. Conversely, Staufen1 regulates migration and invasion of the highly invasive, bone metastatic-derived, PC3 prostate cells via the activation of focal adhesion kinase. Conclusions Collectively, these results show that Staufen1 has a direct impact in prostate cancer development and further demonstrate that its functions vary amongst the prostate cancer cell types. Accordingly, Staufen1 represents a novel target for the development of much-needed therapeutic strategies for prostate cancer.

Neutrophil-Secreted Proteinase 3 Mediates Metastasis of Prostate Cancer Cells Expressing RAGE to the Bone Marrow

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1025-1025 ◽  
Author(s):  
Mikhail Kolonin ◽  
Anna Sergeeva ◽  
Daniela Staquicini ◽  
Jeffrey J. Molldrem ◽  
Renata Pasqualini ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Proteinase 3 ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cell Surfaces

Abstract Human prostate cancer non-randomly metastasizes to the bone marrow, but the biological basis for such site-specific tropism remains largely unresolved. Differential expression of molecules in the bone marrow microenvironment "niche" has recently been proposed to play a role. In previous work, combinatorial selection of random peptide libraries in end-of-life cancer patients has revealed an unexpected interaction between the receptor for advanced glycation end products (RAGE), a molecule expressed on malignant cell surfaces in advanced prostate cancer, and proteinase 3 (PR3), a serine protease abundantly present on neutrophils and promyelocytes within the bone marrow microenvironment. Because RAGE is selectively overexpressed in prostate cancer bone metastases, we hypothesize here that its specific binding to PR3 might mediate homing of prostate cancer cells to the bone marrow. We demonstrate that PR3 non-proteolytically binds to RAGE on prostate cancer cell surfaces and thereby promotes tumor cell activation and motility. We also show that the downstream signal transduction cascade triggered by RAGE/PR3 binding involves p44/42 (Erk1/2) and JNK1 phosphorylation. Finally, we use a mouse model of experimental metastasis to demonstrate that RAGE protein expression on human prostate cancer cells promotes their homing to bone marrow within a short time frame. These results validate a functional protein interaction between RAGE and PR3 and uncover a mechanism through which neutrophils mediate prostate cancer cell metastasis to the skeleton. Disclosures Sergeeva: Astellas: Patents & Royalties. Molldrem:Astellas Pharma: Patents & Royalties.

scholarly journals The impact of Icariside II on human prostate cancer cell proliferation, mobility, and autophagy via PI3K-AKT-mTOR signaling pathway

2020 ◽  
Author(s):  
Shuang Li ◽  
Yunlu Zhan ◽  
Yingwei Xie ◽  
Yonghui Wang ◽  
Yuexin Liu
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
The Impact

Abstract Background The flavonol glycoside icariside Ⅱ (ICA II) has been shown to exhibit a range of anti-tumor properties. Herein we evaluated the impact of ICA II on the proliferation, motility, and autophagy activity of human prostate cancer cells, and we further evaluated the molecular mechanisms underlying these effects. Methods Herein, we treated DU145 human prostate cancer cells with a range of ICA II doses. We then evaluated the proliferative abilities of these cells via CCK-8 assay, whereas apoptosis and cell cycle status were assessed via flow cytometry. We further utilized wound healing and transwell assays to probe the impact of ICA II on migratory and invasive activities, while autophagy was assessed via laser confocal fluorescence microscopy. Western blotting was further utilized to measure LC3-II/I, Beclin-1, P70S6K, PI3K, AKT, mTOR, phospho-AKT, phospho-mTOR, and phospho-P70S6K levels, with RT-PCR being used to evaluate the expression of these same genes at the mRNA level. Results We found that ICA II was capable of mediating a dose- and time-dependent suppression of prostate cancer cell proliferative activity, while also causing these cells to enter a state of cell cycle arrest and apoptosis. We further determined that ICA II treatment was associated with significant impairment of prostate cancer cell migratory and invasive abilities, whereas autophagy was enhanced in treated cells relative to untreated controls. Levels of p-P70S6K, p-mTOR, p-AKT, and PI3K were all also decreased by ICA II. Conclusion Our results indicate that ICA II treatment is capable of suppressing human prostate tumor cell proliferation and disrupting migratory activity while enhancing autophagy through PI3K-AKT-mTOR signaling. As such, ICA II may be an ideal candidate drug for the treatment of prostate cancer.

Attomolar detection of extracellular microRNAs released from living prostate cancer cells by a plasmonic nanowire interstice sensor

Nanoscale ◽  
2017 ◽  
Vol 9 (44) ◽  
pp. 17387-17395 ◽  
Author(s):  
Siyeong Yang ◽  
Hongki Kim ◽  
Kyung Jin Lee ◽  
Seul Gee Hwang ◽  
Eun-Kyung Lim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Human Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines

Extracellular miR141 and miR375 released from living human prostate cancer cell lines were clearly verified by using an extremely sensitive and specific PNI sensor.

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