scholarly journals <i>Toxoplasma gondii</i> But Not <i>Leishmania major</i> or <i>Trichomonas vaginalis</i> Decreases Cell Proliferation and Increases Cell Death on Fibrosarcoma Cancer Cells in Culture Medium

2012 ◽  
Vol 02 (02) ◽  
pp. 105-108 ◽  
Author(s):  
Hedayatollah Shirzad ◽  
Soleiman Khorami ◽  
Narges Soozangar ◽  
Mortaza Yousefi ◽  
Hossein Yousofi Darani
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Toxoplasma Gondii ◽  
Cancer Cells ◽  
Trichomonas Vaginalis ◽  
Culture Medium ◽  
Leishmania Major ◽  
Cells In Culture

scholarly journals Transient Receptor Potential Cation Channels in Cancer Therapy

2019 ◽  
Vol 7 (12) ◽  
pp. 108 ◽  
Author(s):  
Giorgio Santoni ◽  
Federica Maggi ◽  
Maria Beatrice Morelli ◽  
Matteo Santoni ◽  
Oliviero Marinelli
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Transient Receptor

In mammals, the transient receptor potential (TRP) channels family consists of six different families, namely TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPML (mucolipin), TRPP (polycystin), and TRPA (ankyrin), that are strictly connected with cancer cell proliferation, differentiation, cell death, angiogenesis, migration, and invasion. Changes in TRP channels’ expression and function have been found to regulate cell proliferation and resistance or sensitivity of cancer cells to apoptotic-induced cell death, resulting in cancer-promoting effects or resistance to chemotherapy treatments. This review summarizes the data reported so far on the effect of targeting TRP channels in different types of cancer by using multiple TRP-specific agonists, antagonists alone, or in combination with classic chemotherapeutic agents, microRNA specifically targeting the TRP channels, and so forth, and the in vitro and in vivo feasibility evaluated in experimental models and in cancer patients. Considerable efforts have been made to fight cancer cells, and therapies targeting TRP channels seem to be the most promising strategy. However, more in-depth investigations are required to completely understand the role of TRP channels in cancer in order to design new, more specific, and valuable pharmacological tools.

scholarly journals A Potential Antineoplastic Peptide of Human Prostate Cancer Cells Derived from the Lesser Spotted Dogfish (Scyliorhinus canicula L.)

Marine Drugs ◽  
2019 ◽  
Vol 17 (10) ◽  
pp. 585 ◽  
Author(s):  
Adrien Bosseboeuf ◽  
Amandine Baron ◽  
Elise Duval ◽  
Aude Gautier ◽  
Pascal Sourdaine ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Prostate Cancer Cells ◽  
Cell Death Mechanisms ◽  
Autophagy Inhibition

The purpose of the present paper is to investigate the mechanism of action of a pyroglutamate-modified peptide (pE-K092D) on in vitro growth inhibition of MDA-Pca-2b prostate cancer cells. This peptide was derived from a peptide previously isolated from the testis of the lesser spotted dogfish and identified as QLTPEALADEEEMNALAAR (K092D). The effect of the peptide on cell proliferation and cell death mechanisms was studied by flow cytometry. Cellular morphology and cytoskeleton integrity of peptide-treated cells were observed by immunofluorescence microscopy. Results showed the onset of peptide induced early cytoskeleton perturbation, inhibition of autophagy, inhibition of cell proliferation and, at the end, non-apoptotic cell death mechanisms (membrane destabilization and necrosis). All those mechanisms seem to contribute to MDA-Pca-2b growth inhibition by a main cytostatic fate.

Identification of novel 3-nitroacridines as autophagy inducers in gastric cancer cells

2017 ◽  
Vol 41 (10) ◽  
pp. 4087-4095
Author(s):  
Jia Yu ◽  
Xiaoqing Zhao ◽  
Nanmengzi Zhang ◽  
Chaoqun You ◽  
Gang Yao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cells ◽  
Cell Death Pathway ◽  
Gastric Cancer Cell Proliferation

Nine novel 3-nitroacridines were synthesized, of which 3 compounds inhibited gastric cancer cell proliferation via an autophagy-associated cell death pathway.

Effects of nano-taxol/curcumin on ovarian cancer cells

2020 ◽  
Vol 10 (10) ◽  
pp. 1615-1619
Author(s):  
Shuai Zhang ◽  
Junhui Liang ◽  
Changzhong Li ◽  
Fei Wang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Culture Medium ◽  
Morphological Characteristics ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Pharmacodynamic Effect ◽  
Skov3 Cells ◽  
Inhibit Cell Proliferation

To investigate the pharmacodynamic effect of urushin nanoparticles upon the proliferation inhibition in human ovarian cancer SKOV3 cells, and in order to explore their biomechanism, the cell cycle and the percentage of apoptotic cells in human ovarian cancer SKOV3 cells were analyzed utilizing flow cytometry. The concentration of astragalin nanoparticles in SKOV3 cells was identified utilizing HPIC. Consequently, the morphological characteristics of SKOV3 cells in a culture medium of 5 mg/L were investigated and measured. In our findings, the 50 mg cancer cells containing 50 mg IC did not display this noted effect. The results exhibit the discovery that urushin nanoparticles inhibit cell proliferation, which is related to the inhibition of DNA replication and the regulation of the cell proliferation cycle. HPLC results demonstrated that the pharmacological effect of urushin nanoparticles was directly related to the drug concentration present within the studied cells. Hence, urushin nanoparticles can effectively enter cells and then effectively inhibit cell proliferation.

Bimodal effects of platelet-derived growth factor on rat mesangial cell proliferation and death, and the role of lysophosphatidic acid in cell survival

2001 ◽  
Vol 101 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Chiyoko N. INOUE ◽  
Isao NAGANO ◽  
Ryo ICHINOHASAMA ◽  
Natsumi ASATO ◽  
Yoshiaki KONDO ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Growth Factor ◽  
Lysophosphatidic Acid ◽  
Culture Medium ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Platelet Derived Growth Factor ◽  
P53 Expression ◽  
Mesangial Cell Proliferation

Although mesangial cell death has been shown to be correlated with mesangial cell mitosis in vivo, little is known about how these two apparently opposite events are regulated. We show that the addition of platelet-derived growth factor (PDGF; 10–50 ng/ml) to primary cultured rat mesangial cells for 24 h caused continuous proliferation along with simultaneous cell death. This process was accompanied by the fragmentation of DNA into nucleosomal oligomers, the development of apoptotic morphological changes in the nucleus, and increased expression of p53. Accumulation of lactate dehydrogenase (LDH) was also observed in the culture medium, suggesting that both apoptosis and necrosis are involved in the cell death mechanisms observed. We also observed that addition of 30 µM lysophosphatidic acid (LPA) to the culture medium greatly suppressed PDGF-induced cell death, leading to synergistically enhanced mesangial cell proliferation. DNA fragmentation, p53 expression and LDH release were all suppressed by LPA. We suggest that PDGF is a bifunctional molecule in mesangial cells that evokes both cell proliferation and cell death simultaneously, whereas LPA is a survival factor. We speculate that PDGF and LPA may play important roles in the progression or exacerbation of proliferative glomerulonephritis.

scholarly journals Killing tumours by ceramide-induced apoptosis: a critique of available drugs

2003 ◽  
Vol 371 (2) ◽  
pp. 243-256 ◽  
Author(s):  
Norman S. RADIN
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Growth Factors ◽  
Cancer Cells ◽  
Malignant Cells ◽  
Research Papers ◽  
Cell Content ◽  
Sphingosine 1 Phosphate ◽  
Other Substances ◽  
Induced Apoptosis

Over 1000 research papers have described the production of programmed cell death (apoptosis) by interventions that elevate the cell content of ceramide (Cer). Other interventions, which lower cellular Cer, have been found to interfere with apoptosis induced by other agents. Some studies have shown that slowing the formation of proliferation-stimulating sphingolipids also induces apoptosis. These relationships are due to the two different aspects of Cer: Cer itself produces apoptosis, but metabolic conversion of Cer into either sphingosine 1-phosphate or glucosphingolipids leads to cell proliferation. The balance between these two aspects is missing in cancer cells, and yet intervention by stimulating or blocking only one or two of the pathways in Cer metabolism is very likely to fail. This results from two properties of cancer cells: their high mutation rate and the preferential survival of the most malignant cells. Tumours treated with only one or two drugs that elevate Cer can adjust the uncontrolled processes to either maintain or to ‘aggravate’ the excessive growth, angiogenesis and metastasis characteristics of tumours. These treatments might simply elevate the production of growth factors, receptors and other substances that reduce the effectiveness of Cer. Tumour cells that do not adapt in this way undergo apoptosis, leaving the adapted cells free to grow and, ultimately, to ‘subdue’ their host. Thus it is important to kill every type of cancer cell present in the tumour rapidly and simultaneously, using as many different agents to control as many pathways as possible. To aid this approach, this article catalogues many of the drugs that act on different aspects of Cer metabolism. The techniques described here may lead to the development of practical chemotherapy for cancer and other diseases of excess proliferation.

scholarly journals The antimalaria drug artemisinin displays strong cytotoxic effect on leukaemia lymphocytes in combination with vitamin C and pro-vitamin K3

2021 ◽  
Vol 24 (4) ◽  
pp. 533-543
Author(s):  
D. Ivanova ◽  
Z. Yaneva ◽  
R. Bakalova R. Bakalova ◽  
S. Semkova ◽  
Zh. Zhelev
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Vitamin C ◽  
Cancer Cells ◽  
Jurkat Cells ◽  
Cell Counting ◽  
Triple Combination ◽  
Vitamin K3 ◽  
Cell Proliferation Activity ◽  
Proliferation Activity

This study investigated the anticancer effect of the anti-parasitic drug artemisinin in combination with two redox modulators: vitamin C and pro-vitamin K3 (C/K3) The experiments were conducted on leukaemia cells Jurkat. Cells were treated with either artemisinin or C/K3 alone and with all three compounds. Cell proliferation and viability were analysed using trypan blue stating and automated cell counting. The results showed that artemisinin (>10 mM) suppressed cell proliferation activity, but did not induce cell death up to 500 mM. The drug demonstrated a clear cytostatic effect at concentrations 250- 500 mM – Jurkat cells did not proliferate, but were alive. The combination C/K3 (200:2, 300:3 mM/mM) applied alone did not affect cell proliferation and viability. Vitamins C/K3 in concentration ratio 500:5 (μM/mM) decreased cell proliferation activity by ~10%. The triple combination artemisinin/C/K3 manifested synergistic anti-proliferative effects at all concentration ratios analysed. This synergistic effect increased with increasing C/K3 concentration. Based on literature data, it was assumed that the anti-proliferative effect of the triple combination was mediated by changes in the redox-homeostasis of cancer cells. The C/K3 redox system likely acted on cancer mitochondria and increased superoxide production and activation of pro-apoptotic signals, specific for cancer cells. On the other hand, artemisinin could generate hydroxyl radicals as a result of activation of Fenton reactions, depleting intracellular reducing equivalents. Both redox mechanisms lead to activation of signal pathways for induction of cancer cell death.

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