scholarly journals Effects of Long-Term Citrate Treatment in the PC3 Prostate Cancer Cell Line

2019 ◽  
Vol 20 (11) ◽  
pp. 2613 ◽  
Author(s):  
Carmen Caiazza ◽  
Massimo D’Agostino ◽  
Fabiana Passaro ◽  
Deriggio Faicchia ◽  
Massimo Mallardo ◽  
...  

Acute administration of a high level of extracellular citrate displays an anti-proliferative effect on both in vitro and in vivo models. However, the long-term effect of citrate treatment has not been investigated yet. Here, we address this question in PC3 cells, a prostate-cancer-derived cell line. Acute administration of high levels of extracellular citrate impaired cell adhesion and inhibited the proliferation of PC3 cells, but surviving cells adapted to grow in the chronic presence of 20 mM citrate. Citrate-resistant PC3 cells are significantly less glycolytic than control cells. Moreover, they overexpress short-form, citrate-insensitive phosphofructokinase 1 (PFK1) together with full-length PFK1. In addition, they show traits of mesenchymal-epithelial transition: an increase in E-cadherin and a decrease in vimentin. In comparison with PC3 cells, citrate-resistant cells display morphological changes that involve both microtubule and microfilament organization. This was accompanied by changes in homeostasis and the organization of intracellular organelles. Thus, the mitochondrial network appears fragmented, the Golgi complex is scattered, and the lysosomal compartment is enlarged. Interestingly, citrate-resistant cells produce less total ROS but accumulate more mitochondrial ROS than control cells. Consistently, in citrate-resistant cells, the autophagic pathway is upregulated, possibly sustaining their survival. In conclusion, chronic administration of citrate might select resistant cells, which could jeopardize the benefits of citrate anticancer treatment.

Author(s):  
Magdah Ganash

Since the use of engineered antioxidants and antitumor is under investigation, inferable from its likely poisonousness, scientists have deflected their thoughtfulness regarding the quest for characteristic sources to meet the human medication and diet requests. Therefore the study aimed to evaluate the antitumor and antioxidant activities of maize pollen grains against the Prostate Cancer Cell (Pc3) line. Maize pollen grains were collected by Bee through a pollen trap, and then subjected for flavonoids and alkaloids analysis by HPLC method. an in vitro assays, were used to test the antitumor properties, against Pc3 cells. Furthermore, its antioxidant potential was also evaluated by DPPH. The detected flavonoids were identified to be quercetin, luteolin kaempferol, rutin, apigenin and naringin and the alkaloids were quinolone, hydroxyindolenine and conofoline. The antitumor efficacy of pollen grains extract increased with concentration and reached to 94.92 % that similar to the toxicity % of adriamycin at 1000 µg/mL, however, the IC50 (339.81 µg) of pollen grains extract was highest than IC50 (58.07 µg) of adriamycin. At 500 μg/mL of pollen grains extract, morphological changes of Pc3 were recorded. These changes deformed more at 1000 μg/mL. DPPH scavenging activity was found to be 92.26 % at 1280 µg/mL of pollen grains extracted with IC50 425.4 µg/mL compared with IC50 (13.9 µg/mL) of the ascorbic acid. DNA fragmentation and quantitative RT-PCR examinations of Bax and Bcl-2 genes demonstrated that pollen grains extract induced cellular apoptosis of Pc3 cells. This study concluded that the maize pollen grains may applied as natural safe source for inhibit Pc3 Cells proliferation as well as applied as antioxidant.


2021 ◽  
Author(s):  
Alessandra Peres ◽  
Gilson Dorneles ◽  
Gisele Branchini ◽  
Fernanda Nunes ◽  
Pedro Romão ◽  
...  

Abstract This study aimed to evaluate the impact of exercise training plasma on in vitro prostate cancer cell viability and proliferation. PC3 prostate cancer cells were incubated with plasma obtained from young women with high and low physical fitness (PF) and with the plasma collected from institutionalized elderly before and after multimodal exercise training. Plasma from High PF women induced the lowest cell viability and proliferation after incubation time. PC3 cells presented lower cell viability and diminished rates of cell proliferation after the incubation with post-training plasma samples of elderly. The incubation of PC3 cells with post-training plasma of elderly decreased the mitochondrial membrane polarization and increased mitochondrial reactive oxygen species (ROS) production without changes in cytosolic ROS. Post-training plasma did not change apoptosis or necrosis rates in the PC-3 cell line. Multimodal exercise training increased the plasma levels of IL-2, IL-10, IFN-α, and FGF-1, and decreased TNF-α concentrations in institutionalized elderly. In conclusion, we showed that systemic adaptations in plasma mediators of institutionalized elderly may alter cell viability and proliferation by targeting mitochondrial ROS in a prostate cancer cell line.


2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.


Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4181-4191 ◽  
Author(s):  
Brian J. DeBosch ◽  
Maggie Chi ◽  
Kelle H. Moley

Enterocyte fructose absorption is a tightly regulated process that precedes the deleterious effects of excess dietary fructose in mammals. Glucose transporter (GLUT)8 is a glucose/fructose transporter previously shown to be expressed in murine intestine. The in vivo function of GLUT8, however, remains unclear. Here, we demonstrate enhanced fructose-induced fructose transport in both in vitro and in vivo models of enterocyte GLUT8 deficiency. Fructose exposure stimulated [14C]-fructose uptake and decreased GLUT8 protein abundance in Caco2 colonocytes, whereas direct short hairpin RNA-mediated GLUT8 knockdown also stimulated fructose uptake. To assess GLUT8 function in vivo, we generated GLUT8-deficient (GLUT8KO) mice. GLUT8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice. Strikingly, long-term HFrD feeding in GLUT8KO mice exacerbated fructose-induced increases in blood pressure, serum insulin, low-density lipoprotein and total cholesterol vs. wild-type controls. Enhanced fructose uptake paralleled with increased abundance of the fructose and glucose transporter, GLUT12, in HFrD-fed GLUT8KO mouse enterocytes and in Caco2 cultures exposed to high-fructose medium. We conclude that GLUT8 regulates enterocyte fructose transport by regulating GLUT12, and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.


BMC Cancer ◽  
2008 ◽  
Vol 8 (1) ◽  
Author(s):  
Camila ML Machado ◽  
Rafael Y Ikemori ◽  
Tatiana Q Zorzeto ◽  
Ana CMA Nogueira ◽  
Suse DS Barbosa ◽  
...  

2013 ◽  
Vol 14 (7) ◽  
pp. 13577-13591 ◽  
Author(s):  
Wennan Zhao ◽  
Wenzhi Guo ◽  
Qianxiang Zhou ◽  
Sheng-Nan Ma ◽  
Ran Wang ◽  
...  

2020 ◽  
Vol 40 (12) ◽  
Author(s):  
Shunwan Jiang ◽  
Zhi Chen ◽  
Wenqiang Lai ◽  
Qingchun Mai ◽  
Dayu Chen ◽  
...  

Abstract Traditional Chinese medicine (TCM), such as Huanglian-Jie-Du-Tang, a heat-clearing and detoxifying decoction is beneficial for alleviation of inflammation-related diseases. The objective of the present study is to uncover the effect and mechanism of heat-clearing, detoxifying and blood stasis removing decoction (HDBD) on the treatment of acute soft tissue injury (STI) which is characterized with excessive inflammatory cascade at the onset. Male Sprague–Dawley (SD) rats with hammer beating served as the in vivo models of acute STI. Hematoxylin–Eosin (HE) staining was used for histopathology assessment. The levels of inflammatory factors, including prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), interleukin (IL)-1t and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). Human dermal microvascular endothelium cell line HMEC-1 and rat vascular endothelium cell line RAOEC were used to explore the mechanism in vitro. Luciferase gene reporter assay was applied to determine the relationship between miR-26b-5p and Cyclo-oxygenase 2 (COX2). The results showed that HDBD intervention significantly reduced the temperature difference between the healthy side and affected side of rats with hammer beating, together with the decreased levels of COX2, PGE2, TNF-α, IL-6 and IL-1β, and the increased level of miR-26b-5p. In mechanism, miR-26b-5p targeted COX2 and decreased its expression, leading to significant decreases in the levels of PGE2, TNF-α and IL-6 in RAOEC and HMEC-1 cells. In addition, miR-26b-5p inhibition impaired the effects of HDBD on the suppression of PGE2, TNF-α, IL-6 and IL-1β in vitro. In conclusion, the present study revealed that HDBD relieved acute STI via modulating miR-26b-5p/COX2 axis to inhibit inflammation.


2018 ◽  
Vol 50 ◽  
pp. 305-317 ◽  
Author(s):  
L. Galbis-Martínez ◽  
M.L. Fernández-Cruz ◽  
L. Alte ◽  
A. Valdehita ◽  
I. Rucandio ◽  
...  

Author(s):  
J. S. DILEEP KUMAR ◽  
JAYA PRABHAKARAN ◽  
NARESH DAMUKA ◽  
JUSTIN W. HINES ◽  
STEVEN J. KRIDEL ◽  
...  

Objective: The objective of this study was to evaluate the uptake and specificity of [11C]MPC-6827, a MT targeted PET ligand in prostate, glioblastoma and breast cancer cells. Methods: [11C]MPC-6827 was synthesized by reacting corresponding desmethyl precursors with [11C]CH3I in a GE-FX2MeI/FX2M radiochemistry module. In vitro binding of [11C]MPC-6827 was performed in breast cancer MDA-MB-231, glioblastoma (GBM) patient-derived tumor (GBM-PDX), GBM U251 and prostate cancer 3 (PC3) cell lines at 37 °C in quadruplicate at 5, 15, 30, 60, and 90 minute incubation time. The nonspecific bindings were determined by incubation with unlabeled microtubule targeting agents MPC-6827, HD-800, colchicine, paclitaxel and docetaxel (5.0 mM). Results: [11C]MPC-6827 provided the highest binding in the breast cancer cell, MDA-MB-231, among all the cells studied, with 90% specific binding. [11C]MPC-6827 binds to glioblastoma PDX and U251 cells with ~50% and 40% specific binding, whereas, prostate cancer cell line, PC3 cells showed 40% specific binding. [11C]MPC-6827 also exhibits binding to the taxane and colchicine binding sites of MTs, in MDA-MB-231 cells. Conclusion: These data indicate that [11C]MPC-6827 can be a promising PET radiotracer for preclinical imaging of the brain and peripheral cancers.


Sign in / Sign up

Export Citation Format

Share Document