scholarly journals Mechanism of Ferritin Heavy Chain in the Proliferation and Migration of Prostate Cancer Cells

2021 ◽  
Author(s):  
Cuixiu Lu ◽  
Huijun Zhao ◽  
Man Zhang
Keyword(s):  
Prostate Cancer ◽  
Mass Spectrometry ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Heavy Chain ◽  
Prostate Cancer Cell ◽  
Prostate Cancer Cell Lines ◽  
Ferritin Heavy Chain ◽  
And Migration

Abstract Ferritin is an important molecule in the regulation of cell proliferation, growth inhibition escape, cell death inhibition and angiogenesis. More and more studies have given evidence of abnormal iron metabolism in tumors. Whether ferritin can be a new type of marker for early diagnosis of tumorous diseases remains to be explored. In this study, we verified the expression level of ferritin heavy chain (FTH) in benign prostatic hyperplasia epithelial cell (BPH-1) and three kinds of PCa cells by Western blotting. Lentivirus was used to construct FTH gene overexpression vector, then construct FTH overexpression PCa cell lines. Meanwhile, LNCaP cells and DU145 cells FTH silent expression prostate cancer cell lines were constructed using Crispr Cas9 technology. Next, clone proliferation experiments, transwell experiments, and scratch experiments were used to verify the cell proliferation, invasion, and migration capabilities of each group of cells with different FTH expression levels. The FTH knockout PC-3 cell (LV-shFTH PC3) has been established in our laboratory. Make full use of the existing results from Isobaric Tag for Relative and Absolute Quantitation (iTRAQ) mass spectrometry technology to analyze differentially expressed protein analysis between LV-shFTH PC3 cells and control cells. Combine GO analysis to select the target protein for subsequent cell protein expression level verification. Our results show that FTH overexpression can promote the proliferation, migration and invasion of prostate cancer cell lines, while FTH knockout causes the opposite result. Combined with mass spectrometry (MS) detection, it is speculated that FTH may trigger changes in cell behavior by regulating the expression of the following proteins: S100A4, CRABP1, S100A2, S100P, GDF15, FAM84B, KRT75, LYRM7, OCLN, LCP1, F2RL1. (The study is not a clinical trial, no registration number and registration date are required)

In vitro efficacy of MAGMAS inhibition in prostate cancer.

2014 ◽  
Vol 32 (4_suppl) ◽  
pp. 281-281
Author(s):  
Benjamin C. Powers ◽  
Bhaskar Das ◽  
Boumediene Bouzahzah ◽  
Peter J. Van Veldhuizen ◽  
Emma Borrego-Diaz Reyes
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines ◽  
Gm Csf ◽  
Androgen Independent

281 Background: Prostate cancer is the second most common cancer worldwide in males. The initial treatment in advanced cases is medical or surgical castration. The outlook declines when prostate cancer advances independently, despite the aforementioned castration. Within the last ten years, a handful of new agents have proven effective in this castration-resistant phase, but finding more effective, novel ways of treating advanced prostate cancer is warranted. MAGMAS (mitochondria-associated, granulocyte-macrophage colony stimulating factor (GM-CSF) signaling molecule) is a protein ubiquitously expressed in eukaryotic cells that plays a key role in embryonal development in a variety of species. Overexpression of MAGMAS has anti-apoptotic effects, as GM-CSF is a growth factor essential for survival, proliferation and differentiation of cells. MAGMAS and GM-CSF receptor levels have been shown to be overexpressed in prostate cancer, but do not correlate with pathological grade or clinical stage. The purpose of our study was to evaluate the efficacy of a MAGMAS inhibitor, synthesized by Dr Bhaskar Das, in androgen-dependent and androgen-independent prostate cancer cell lines, as well as in a normal prostate cell line as another control. Methods: The different cell lines were treated with MAGMAS inhibitor at various concentrations in vitro. For analysis, we used MTT Cell Proliferation assay at 24 and 48 hours, per manufacturer’s protocol. We tested MAGMAS inhibitor effect on apoptosis/necrosis, cell migration and microtubule destabilization as well. Results: After prostate cancer cell lines were treated with MAGMAS inhibitor in vitro, cell proliferation and migration decreased, apoptosis and necrosis were induced, and microtubules were destabilized, all showing more impressive results in the androgen-independent cells. MAGMAS inhibition did not affect cell proliferation in the normal prostate cells. Conclusions: In vitro studies show MAGMAS inhibition proves efficacious in both androgen-dependent and androgen-independent prostate cancer cell lines. This will be evaluated further in a xenograft mouse model.

scholarly journals Expression of Human Prostatic Acid Phosphatase Correlates with Androgen-stimulated Cell Proliferation in Prostate Cancer Cell Lines

1998 ◽  
Vol 273 (10) ◽  
pp. 5939-5947 ◽  
Author(s):  
Ming-Fong Lin ◽  
Tzu-Ching Meng ◽  
Prathibha S. Rao ◽  
Chawnshang Chang ◽  
Axel H. Schönthal ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Acid Phosphatase ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Prostatic Acid Phosphatase ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines

Slug/SNAI2 regulates cell proliferation and invasiveness of metastatic prostate cancer cell lines

Tumor Biology ◽  
2010 ◽  
Vol 31 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Modjtaba Emadi Baygi ◽  
Zahra-Soheila Soheili ◽  
Frank Essmann ◽  
Abdolkhaleg Deezagi ◽  
Rainer Engers ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Metastatic Prostate Cancer ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cell Lines

scholarly journals SIRT4 Overexpression Promotes the Inhibition of Cell Proliferation and Invasion in Prostate Cancer

2020 ◽  
pp. 276-284
Author(s):  
Abdul-Nazif Mahmud ◽  
Feilun Cui ◽  
Xue Bo ◽  
Jianpeng Hu ◽  
Tingjun Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Tumor ◽  
Prostate Cancer Cell Lines ◽  
Proliferation And Invasion

<p><strong>Background:</strong> SIRT4 is among the few characterized individual sirtuin groups of nicotinamide adenine dinucleotide-dependent enzymes base in the mitochondria that facilitate several significant processes at the cellular level including stress response, metabolism and longevity. SIRT4 can suppress and inhibits the growth, proliferation and transformation of tumor cells such as colorectal and gastric tumors by suppressing glutamine anaplerosis, but there is no research that reveal the role and function SIRT4 plays in the development of prostate tumor.</p> <p><strong>Methods:</strong> Overexpression of SIRT4 in prostate cancer cell lines LNCaP was determined using RT-qPCR and Western blotting analyses. CCK-8 and transwell analysis were utilized to establish SIRT4 overexpression effects on cell proliferation and cell invasion respectively.</p> <p><strong>Results:</strong> This study first established SIRT4 overexpression in prostate cancer cell lines LNCaP, functional experiment such as CCK-8 assay reveals that, overexpression of SIRT4 suppressed cell proliferation. In addition, transwell assay reveals that, SIRT4 overexpression inhibits cell invasion.</p> <p><strong>Conclusions:</strong> This research findings reveals that, SIRT4 function to suppress prostate cancer cells by impeding the proliferation and invasion of LNCaP cells. SIRT4 may serve as a new treatment target for prostate tumor.</p>

Sign in / Sign up

Export Citation Format

Share Document