scholarly journals Strigolactone analogues induce apoptosis through activation of p38 and the stress response pathway in cancer cell lines and in conditionally reprogrammed primary prostate cancer cells.

Oncotarget ◽  
2014 ◽  
Vol 5 (6) ◽  
pp. 1683-1698 ◽  
Author(s):  
Claire B Pollock ◽  
Sara McDonough ◽  
Victor S. Wang ◽  
Hyojung Lee ◽  
Lymor Ringer ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stress Response ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Primary Prostate Cancer ◽  
Stress Response Pathway

scholarly journals Identifying metastatic ability of prostate cancer cell lines using native fluorescence spectroscopy and machine learning methods

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jianpeng Xue ◽  
Yang Pu ◽  
Jason Smith ◽  
Xin Gao ◽  
Chun Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Machine Learning ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Cell Lines ◽  
Native Fluorescence

AbstractMetastasis is the leading cause of mortalities in cancer patients due to the spreading of cancer cells to various organs. Detecting cancer and identifying its metastatic potential at the early stage is important. This may be achieved based on the quantification of the key biomolecular components within tissues and cells using recent optical spectroscopic techniques. The aim of this study was to develop a noninvasive label-free optical biopsy technique to retrieve the characteristic molecular information for detecting different metastatic potentials of prostate cancer cells. Herein we report using native fluorescence (NFL) spectroscopy along with machine learning (ML) to differentiate prostate cancer cells with different metastatic abilities. The ML algorithms including principal component analysis (PCA) and nonnegative matrix factorization (NMF) were used for dimension reduction and feature detection. The characteristic component spectra were used to identify the key biomolecules that are correlated with metastatic potentials. The relative concentrations of the molecular spectral components were retrieved and used to classify the cancer cells with different metastatic potentials. A multi-class classification was performed using support vector machines (SVMs). The NFL spectral data were collected from three prostate cancer cell lines with different levels of metastatic potentials. The key biomolecules in the prostate cancer cells were identified to be tryptophan, reduced nicotinamide adenine dinucleotide (NADH) and hypothetically lactate as well. The cancer cells with different metastatic potentials were classified with high accuracy using the relative concentrations of the key molecular components. The results suggest that the changes in the relative concentrations of these key fluorophores retrieved from NFL spectra may present potential criteria for detecting prostate cancer cells of different metastatic abilities.

scholarly journals Bee Venom Components as Therapeutic Tools against Prostate Cancer

Toxins ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 337
Author(s):  
Jasmin Katrin Badawi
Keyword(s):  
Prostate Cancer ◽  
Side Effects ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Therapeutic Agents ◽  
Bee Venom ◽  
Surrounding Tissue ◽  
Prostate Cancer Cells

Prostate cancer is one of the most common cancers in men. Despite the development of a variety of therapeutic agents to treat either metastatic hormone-sensitive prostate cancer, advanced prostate cancer, or nonmetastatic/metastatic castration-resistant prostate cancer, the progression or spread of the disease often cannot be avoided. Additionally, the development of resistance of prostate cancer cells to available therapeutic agents is a well-known problem. Despite extensive and cost-intensive research over decades, curative therapy for metastatic prostate cancer is still not available. Therefore, additional therapeutic agents are still needed. The animal kingdom offers a valuable source of natural substances used for the treatment of a variety of diseases. Bee venom of the honeybee is a mixture of many components. It contains proteins acting as enzymes such as phospholipase A2, smaller proteins and peptides such as melittin and apamin, phospholipids, and physiologically active amines such as histamine, dopamine, and noradrenaline. Melittin has been shown to induce apoptosis in different cancer cell lines, including prostate cancer cell lines. It also influences cell proliferation, angiogenesis, and necrosis as well as motility, migration, metastasis, and invasion of tumour cells. Hence, it represents an interesting anticancer agent. In this review article, studies about the effect of bee venom components on prostate cancer cells are discussed. An electronic literature research was performed utilising PubMed in February 2021. All scientific publications, which examine this interesting subject, are discussed. Furthermore, the different types of application of these promising substances are outlined. The studies clearly indicate that bee venom or melittin exhibited anticancer effects in various prostate cancer cell lines and in xenografts. In most of the studies, a combination of bee venom or the modified melittin with another molecule was utilised in order to avoid side effects and, additionally, to target selectively the prostate cancer cells or the surrounding tissue. The studies showed that systemic side effects and unwanted damage to healthy tissue and organs could be minimised when the anticancer drug was not activated until binding to the cancer cells or the surrounding tissue. Different targets were used, such as the matrix metalloproteinase 2, hormone receptors expressed by prostate cancer cells, the extracellular domain of PSMA, and the fibroblast activation protein occurring in the stroma of prostate cancer cells. Another approach used loaded phosphate micelles, which were cleaved by the enzyme secretory phospholipase A2 produced by prostate cancer cells. In a totally different approach, targeted nanoparticles containing the melittin gene were used for prostate cancer gene therapy. By the targeted nonviral gene delivery, the gene encoding melittin was delivered to the prostate cancer cells without systemic side effects. This review of the scientific literature reveals totally different approaches using bee venom, melittin, modified melittin, or protoxin as anticancer agents. The toxic agents acted through several different mechanisms to produce their anti-prostate cancer effects. These mechanisms are not fully understood yet and more experimental studies are necessary to reveal the complete mode of action. Nevertheless, the researchers have conducted pioneering work. Based on these results, further experimental and clinical studies about melittin and modifications of this interesting agent deriving from nature are necessary and could possibly lead to a complementary treatment option for prostate cancer.

scholarly journals COMPARATIVE IN-VITRO ANTICANCER ACTIVITY OF THANGA PARPAM (SIDDHA GOLD DRUG) IN BREAST, LIVER, PROSTATE AND LUNG CANCER CELL LINES

2021 ◽  
Vol 12 (1) ◽  
pp. 64-67
Author(s):  
Sulthan Shajahan ◽  
Arul Amuthan
Keyword(s):  
Prostate Cancer ◽  
Lung Cancer ◽  
Particle Size ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells

Thanga parpam is a gold nanoparticle used in Siddha for many chronic and challenging diseases including cancers. Clinically it shows benefit in some cancer types, but not to all types. This study was aimed to compare the in-vitro anticancer activity of Thanga parpam in various cancer cell lines. The particle size and elements were evaluated using Scanning Electron Microscope coupled with Energy Dispersive X-Ray Spectroscopy. Thanga parpam was added to breast adenocarcinoma cells, Human hepatocellular carcinoma cells, Human prostate cancer cells and Human lung adenocarcinoma epithelial cells for 24 hours. MTT assay was used to evaluate the cell viability. Graph was drawn from the % cell viability and dose required to kill 50 % cells was calculated. The gold particles are irregular disk shaped, but agglomerated to each other and not in uniform size. The particle size varies from 17.8 nm – 448 nm. About 9.3% of gold element was present in oxide and sulfide form. It showed dose dependent killing effect on all cancer cell lines. IC50% value was 0.63, 3.51, 6.65 and 11.01 µg/ml for breast, liver, prostate and lung cancer cells respectively. Thanga parpam is a potent anticancer drug to all the four cancer cells, however higher efficacy was observed in breast, liver and prostate cancer cells.

scholarly journals Expression and action of the growth hormone releasing peptide ghrelin and its receptor in prostate cancer cell lines

2002 ◽  
Vol 172 (3) ◽  
pp. R7-11 ◽  
Author(s):  
PL Jeffery ◽  
AC Herington ◽  
LK Chopin
Keyword(s):  
Prostate Cancer ◽  
Growth Hormone ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cancer Cell Lines

This study has examined the expression of two new facets of the growth hormone axis, the growth hormone secretagogue receptor (GHS-R) and its recently identified putative natural ligand ghrelin, in prostate cancer cells. GHS-R 1a and 1b isoforms and ghrelin mRNA expression were detected by RT-PCR in the ALVA-41, LNCaP, DU145 and PC3 prostate cancer cell lines. A normal prostate cDNA library expressed GHS-R1a, but not the 1b isoform or ghrelin. Immunohistochemical staining for the GHS-R 1a isoform and ghrelin was positive in the four cell lines studied. PC3 cells showed increased cell proliferation in vitro in response to ghrelin to levels 33% above untreated controls, implying a potential tumour-promoting role for ghrelin in this tissue. This study is the first to demonstrate the co-expression of the GHS-R and ghrelin in prostate cancer cells. It is also the first study to provide evidence that a previously unrecognised autocrine/paracrine pathway involving ghrelin, that is capable of stimulating growth, exists in prostate cancer.

scholarly journals ZBTB38 suppresses prostate cancer cell proliferation and migration via directly promoting DKK1 expression

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Guanxiong Ding ◽  
Wei Lu ◽  
Qing Zhang ◽  
Kai Li ◽  
Huihui Zhou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Target Genes ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Cell Lines ◽  
Interacting Protein

AbstractProstate cancer is still one of the most common malignancies in men all around the world. The mechanism of how prostate cancer initiates and develops is still not clear. Here in this study, we show that tumor suppressor ZBTB38 could suppress the migration and proliferation of prostate cancer cells. We find lower ZBTB38 expression in prostate cancer tissues, which also strongly predicts a poorer prognosis of prostate cancer. ZBTB38 binds DKK1 (Dickkopf WNT signaling pathway inhibitor 1) locus and promotes DKK1 expression in prostate cancer cell lines. Consistently, reduction of DKK1 expression significantly restores ZBTB38-mediated suppression of migration and proliferation of prostate cancer cell lines. Mechanistically, we find that ZBTB38 primarily binds the promoters of target genes, and differentially regulates the expression of 1818 genes. We also identify PRKDC (protein kinase, DNA-activated, catalytic subunit) as a ZBTB38-interacting protein that could repress the function of ZBTB38 in suppressing migration and proliferation of prostate cancer cells. Taken together, our results indicate that ZBTB38 could repress cell migration and proliferation in prostate cancer via promoting DKK1 expression, and also provide evidence supporting ZBTB38 as a potential prognosis marker for prostate cancer.

scholarly journals PLK1 downregulation by RO3280 prevents cell proliferation, migration, and invasion via the Wnt/β-catenin pathway in prostate cancer

2021 ◽  
Author(s):  
Yongxue Ding ◽  
Zhe Zhang ◽  
Min Ju
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Real Time ◽  
Cell Lines ◽  
Cancer Cell ◽  
Western Blotting ◽  
Cancer Cell Lines ◽  
Migration And Invasion ◽  
Prostate Cancer Cells

IntroductionHigher expression levels of serine/threonine-protein kinase 1 (PLK1) are significantly associated with tumorigenesis and poor clinical prognoses. Consequently, PLK1 is considered a latent target in cancer treatment. We aimed to determine the cytotoxic effects of RO3280 on prostate cancer cells.Material and methodsPLK1 expression was investigated using real-time PCR and western blotting in prostate cancer tissues and paired normal tissues. Real-time cell analysis, cell counting kit-8 assays, and 5-ethynyl-2¢-deoxyuridine cell proliferation assays were applied for the examination of cell proliferation ability. Wound healing assays and transwell assays were used to assess the migratory and invasive abilities of the prostate cancer cell lines with or without RO3280 treatment. Moreover, the target genes and pathways were detected by transcriptomics RNA sequencing in the cells cultured in RO3280 and through a series of bioinformatics analyses. Finally, the Wnt/β-catenin pathway was screened out and verified by western blotting.ResultsWe observed the mRNA and protein overexpression of PLK1 in the prostate cancer cells and tissues. The inhibition of PLK1 by RO3280 significantly reduced the migratory, invasive, and proliferative properties of the RO3280-treated cancer cell lines compared with their controls. RO3280 mediated the inactivation of the Wnt/β-catenin pathway, and reduced the rates of cell proliferation, migration, and invasion in prostate cancer cells.ConclusionsThis study’s findings are significant owing to the identification of the specific anticancer mechanism of RO3280, which may have therapeutic effects. This trial provides clarity on the feasibility of the use of RO3280 as a cancer therapeutic agent for prostate cancer.

scholarly journals Circular RNA circ_0057558 Controls Prostate Cancer Cell Proliferation Through Regulating miR-206/USP33/c-Myc Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Tao Ding ◽  
Yanjun Zhu ◽  
Huimin Jin ◽  
Ping Zhang ◽  
Jianming Guo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Negative Correlation ◽  
Bioinformatics Analysis ◽  
Prostate Cancer Cell ◽  
Prostate Cancer Cells ◽  
Cancer Tissues

We previously reported the elevated expression of circ_0057558 in prostate cancer tissues and cell lines. Here, we aimed to determine the biological function of circ_0057558 in prostate cancer. In the current study, circ_0057558 knockdown in prostate cancer cells significantly repressed cell proliferation and colony formation, but promoted cell arrest and enhanced the sensitivity to docetaxel. Bioinformatics analysis prediction and RNA-pull down assay identified miR-206 as the potential binding miRNA of circ_0057558. A negative correlation was observed between the expression of miR-206 and circ_0057558 in prostate cancer tissues. miR-206 mimics rescued the function of circ_0057558 overexpression on prostate cancer cells. Further, the bioinformatics analysis and luciferase assay suggested that miR-206 may target ubiquitin-specific peptidase 33 (USP33). USP33 mRNA expression has negative correlation with miR-206 expression and positive correlation with circ_0057558 expression in prostate cancer tissues. USP33 overexpression partially blocked the effects of miR-206 mimics on prostate cell proliferation. USP33 could bind and deubiquitinate c-Myc. Increased c-Myc protein by circ_0057558 overexpression was partially reversed by miR-206 mimics. The proliferation inhibition activity of MYC inhibitor 361 (MYCi361) was more prominent in primary prostate cancer cells and patient-derived xenograft (PDX) model with higher level of circ_0057558. Collectively, circ_0057558 gives an impetus to cell proliferation and cell cycle control in prostate cancer cell lines by sponging miR-206 and positively regulating the transcription of the miR-206 target gene USP33.

scholarly journals ZFP91: A Noncanonical NF-κB Signaling Pathway Regulator with Oncogenic Properties Is Overexpressed in Prostate Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Lukasz Paschke ◽  
Karol Jopek ◽  
Marta Szyszka ◽  
Marianna Tyczewska ◽  
Agnieszka Ziolkowska ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Biology ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Mrna Levels ◽  
Prostate Cancer Cell Lines

Novel molecular targets are being searched to aid in prostate cancer diagnosis and therapy. Recently, ZFP91 zinc finger protein has been found to be upregulated in prostate cancer cell lines. It is a potentially important oncogenic protein; however only limited data regarding its biological function and expression patterns are available. To date, ZFP91 has been shown to be a key factor in activation of noncanonical NF-κB signaling pathway as well as to be involved in HIF-1α signaling in cancer cells. The present study aimed to characterize ZFP91 expression in prostate cancer specimens. Furthermore, since our earlier reports showed discrepancies between ZFP91 mRNA and protein levels, we studied this interrelationship in LNCaP and PC-3 prostate cancer cell lines using siRNA mediated knockdown. QPCR analysis revealed marked upregulation of ZFP91 mRNA in the majority of prostate cancer specimens. Transfection of prostate cancer cells with ZFP91 siRNA resulted in a 10-fold decrease in mRNA levels. On a protein level, however, no inhibitory effect was observed over the time of the cell culture. We conclude that ZFP91 is overexpressed in prostate cancer and that potential accumulation of the ZFP91 protein in studied cells may be of importance in prostate cancer biology.

scholarly journals Effect of 1-Carbaldehyde-3,4-dimethoxyxanthone on Prostate and HPV-18 Positive Cervical Cancer Cell Lines and on Human THP-1 Macrophages

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3721
Author(s):  
Rui Medeiros ◽  
Bruno Horta ◽  
Joana Freitas-Silva ◽  
Jani Silva ◽  
Francisca Dias ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Metabolic Activity ◽  
Cancer Cell Lines ◽  
No Production ◽  
Prostate Cell ◽  
Raw264.7 Macrophages

Xanthone derivatives have shown promising antitumor properties, and 1-carbaldehyde-3,4-dimethoxyxanthone (1) has recently emerged as a potent tumor cell growth inhibitor. In this study, its effect was evaluated (MTT viability assay) against a new panel of cancer cells, namely cervical cancer (HeLa), androgen-sensitive (LNCaP) and androgen-independent (PC-3) prostate cancer, and nonsolid tumor derived cancer (Jurkat) cell lines. The effect of xanthone 1 on macrophage functions was also evaluated. The effect of xanthone 1-conditioned THP-1 human macrophage supernatants on the metabolic viability of cervical and prostate cancer cell lines was determined along with its interference with cytokine expression characteristic of M1 profile (IL-1 ≤ β; TNF-α) or M2 profile (IL-10; TGF-β) (PCR and ELISA). Nitric oxide (NO) production by murine RAW264.7 macrophages was quantified by Griess reaction. Xanthone 1 (20 μM) strongly inhibited the metabolic activity of the cell lines and was significantly more active against prostate cell lines compared to HeLa (p < 0.05). Jurkat was the cell most sensitive to the effect of xanthone 1. Compound 1-conditioned IL-4-stimulated THP-1 macrophage supernatants significantly (p < 0.05) inhibited the metabolic activity of HeLa, LNCaP, and PC-3. Xanthone 1 did not significantly affect the expression of cytokines by THP-1 macrophages. The inhibiting effect of compound 1 observed on the production of NO by RAW 264.7 macrophages was moderate. In conclusion, 1-carbaldehyde-3,4-dimethoxyxanthone (1) decreases the metabolic activity of cancer cells and seems to be able to modulate macrophage functions.

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