scholarly journals A possible relation between dietary zinc and cAMP in the regulation of tumour cell proliferation in the rat

1988 ◽  
Vol 59 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Noel S. Skeef ◽  
John R. Duncan
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Cell Line ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Zn Deficiency ◽  
Regenerating Liver ◽  
Small Reduction ◽  
Dietary Zinc ◽  
Camp Concentration

1. The possibility of an effect of zinc on the rate of tumour cell division, mediated through a regulation of cellular cAMP concentration, was investigated in the present study in rats.2. Dietary Zn deficiency (< 1·5 mg Zn/kg) but not Zn excess (500 mg Zn/kg) resulted in an increased cAMP concentration in transplanted hepatoma cells. Neither treatment had any effect on the cAMP concentration in regenerating liver or normal resting liver. Both the deficient and excess Zn diets resulted in a small reduction in tumour growth (not statistically significant).3. The results seem to indicate that the relation investigated in the present study does not apply in the cell line used.

scholarly journals Differences in tumour growth, tumour cell proliferation and immune function after laparoscopy and laparotomy in an animal model

HPB ◽  
2001 ◽  
Vol 3 (3) ◽  
pp. 213-217 ◽  
Author(s):  
A.G. Lopes ◽  
C.J. Rodrigues ◽  
L.H. Lopes ◽  
H. Vilca‐Melendez ◽  
A.J. Rodrigues
Keyword(s):  
Cell Proliferation ◽  
Animal Model ◽  
Immune Function ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Tumour Cell Proliferation

β-Eudesmol suppresses tumour growth through inhibition of tumour neovascularisation and tumour cell proliferation

2008 ◽  
Vol 10 (2) ◽  
pp. 159-167 ◽  
Author(s):  
EN-LONG Ma ◽  
YAN-CHUN Li ◽  
HIROSHI Tsuneki ◽  
JIN-FANG Xiao ◽  
MING-YU Xia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Tumour Cell Proliferation

scholarly journals Effects of Ursolic Acid and its Analogues on Soybean 15-Lipoxygenase Activity and the Proliferation Rate of A human Gastric Tumour Cell Line

1994 ◽  
Vol 3 (3) ◽  
pp. 181-184 ◽  
Author(s):  
D. Es-Saady ◽  
A. Najid ◽  
A. Simon ◽  
Y. Denizot ◽  
A. J. Chulia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Ursolic Acid ◽  
Oleanolic Acid ◽  
Tumour Cell ◽  
Lipoxygenase Activity ◽  
Tumour Cell Line ◽  
Dependent Manner ◽  
Gastric Tumour ◽  
Methyl Ursolate

The authors have previously isolated and purified ursolic acid from heather flowers (Calluna vulgarts). This terpene was found to inhibit HL-60 leukaemic cell proliferation and arachidonic acid oxidative metabolism in various cell species. The effects of ursolic acid and its analogues on soybean 15-lipoxygenase activity and on the proliferation of a human gastric tumour cell line (HGT), have been assessed. These triterpenes inhibited soybean 15-lipoxygenase at its optimal activity (pH 9). The proliferation ofHGT was decreased in a dose-dependent manner. At 20 μM the rank order is: ursolic acid > uvaol > oleanolic acid > methyl ursolate. The carboxylic group at the C28position of ursolic acid appears to be implicated in the inhibition of both lipoxygenase activity and cell proliferation. Thus methylation of this group decreases these two inhibitory properties. Oleanolic acid, which differs by the position of one methyl group (C20instead of C19) is less inhibitory than ursolic acid. The lipophilicity of the terpene is also implicated since uvaol appears to be more inhibitory than methyl ursolate.

scholarly journals In situApoptotic and Proliferation Index in Laryngeal Squamous Cell Carcinomas

1998 ◽  
Vol 16 (3) ◽  
pp. 177-184 ◽  
Author(s):  
Hjalmar G. Hagedorn ◽  
Jutta Tübel ◽  
Irmgard Wiest ◽  
Andreas G. Nerlich
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Proliferation Index ◽  
Strong Increase ◽  
Tumour Stroma ◽  
Ki 67 ◽  
Laryngeal Mucosa ◽  
Proliferation And Apoptosis

The rate of cellular growth is mainly influenced by the balance between cell proliferation and cellular decay. Since to our knowledge, no study so far has analysed the rate of proliferation and apoptosis in the normal laryngeal mucosa and in invasive laryngeal carcinomas, we performed a morphological analysis on both parameters in biopsies from 30 patients with laryngeal carcinoma. We applied the TUNEL end labelling technique for the investigation of apoptosis and immunohistochemistry (Ki‐67 antigen) for the determination of the cell proliferation.In our study we demonstrated that invasive tumour growth of the larynx coincides with an increase of both cellular proliferation and apoptosis. Both parameters, however, affected various tumour areas differently. While there was a preferential expression of the Ki‐67 antigen at the tumour–stroma interface, apoptotic figures could be found randomly distributed in the tumour. This indicates that the replication of tumour cells and tumour cell decay are differently distributed and possibly independently regulated. Since we observed a particularly strong increase of cell proliferation at the tumour–stroma interface which outnumbered the corresponding rate of apoptosis by far, the enhanced cell proliferation at the tumour border seems to be a main factor for tumour growth.A statistical evaluation revealed significant correlation between the apoptotic index and the degree of tumour cell differentiation, indicating that a high rate of apoptosis coincides with a high level of tumour cell differentiation.There was, however, no statistically significant correlation between prognostic clinical parameters and the rate of apoptosis or that of proliferation.

Chemokines in cancer

2001 ◽  
Vol 3 (19) ◽  
pp. 1-18 ◽  
Author(s):  
Mitchell J. Frederick ◽  
Gary L. Clayman
Keyword(s):  
Cell Proliferation ◽  
Mouse Models ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Inflammatory Responses ◽  
Immunological Response ◽  
Direct Stimulation ◽  
Cancer Intervention ◽  
Pleiotropic Functions ◽  
Stimulation Of

Chemokines are small, chemotactic cytokines that direct migration of leukocytes, activate inflammatory responses and participate in many other pleiotropic functions, including regulation of tumour growth. Chemokines modulate tumour behaviour by three important mechanisms: regulation of tumour-associated angiogenesis, activation of a host tumour-specific immunological response, and direct stimulation of tumour cell proliferation in an autocrine fashion. All of these mechanisms are promising points of cancer intervention, and preclinical mouse models suggest that chemokine antagonists and agonists could become important in the development of new anticancer therapies.

HIF1A is Overexpressed in Medulloblastoma and its Inhibition Reduces Proliferation and Increases EPAS1 and ATG16L1 Methylation

2018 ◽  
Vol 18 (3) ◽  
pp. 287-294 ◽  
Author(s):  
Gustavo Alencastro Veiga Cruzeiro ◽  
Maristella Bergamo dos Reis ◽  
Vanessa Silva Silveira ◽  
Regia Caroline Peixoto Lira ◽  
Carlos Gilberto Carlotti Jr ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Cellular Proliferation ◽  
Mrna Level ◽  
Relevant Information ◽  
Protein Stabilization ◽  
Mrna Levels ◽  
Medulloblastoma Cell Line ◽  
Pediatric Medulloblastoma ◽  
Fresh Frozen

Background: Genetic and epigenetic modifications are closely related to tumor initiation and progression and can provide guidance for understanding tumor functioning, potentially leading to the discovery of new therapies. Studies have associated hypoxia-related genes to tumor progression and chemo/radioresistance in brain tumors. Information on the expression profile of hypoxiarelated genes in pediatric medulloblastoma, although scarce, may reveal relevant information that could support treatment decisions. Objective: Our study focused on evaluation the of CA9, CA12, HIF1A, EPAS1, SCL2A1 and VEGF genes in 41 pediatric fresh-frozen medulloblastoma sample. Additionally, we analyzed the effect of hypoxia and normoxia in the pediatric medulloblastoma cell-line UW402. Furthermore, we assessed the effects of HIF1A knockdown in cell-proliferation and methylation levels of genes related to hypoxia, apoptosis and autophagy. Method: qPCR was performed to evaluate mRNA levels, and Western blot to confirm HIF1A silencing in both patient samples and cell line. Pyrosequencing was performed to asses the methylation levels after HIF1A knockdown in the UW402 cell line. Results: A higher HIF1A mRNA level was observed in MB patients when compared to the cerebellum (non-tumor match). In UW402 MB cell-line, chemically induced hypoxic resulted in an increase of mRNA levels of HIF1A, VEGF, SCL2A1 and CA9 genes. Additionally, HIF1A knockdown induced a decrease in the expression of hypoxia related genes and a decrease of 30% in cell proliferation was also observed. Also, a significant increase in the methylation of ATG16L1 promoter and decrease in the methylation of EPAS1 promoter were observed after HIF1A knockdown. Conclusion: HIF1A knockdown in medulloblastoma cells lead to decreased cellular proliferation, suggesting that HIF1A can be a potential therapeutic target to be explored in the medulloblastoma. However, the mechanisms behind HIF1A protein stabilization and function are very complex and more data need to be generated to potentially use HIF1A as a therapeutical target.

Statins: A Conceivable Remedial Role for the Regulation of Cancer Progression

2019 ◽  
Vol 15 (2) ◽  
pp. 131-145
Author(s):  
Gajanan V. Sherbet
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Tumour Growth ◽  
Cell Function ◽  
Mevalonate Pathway ◽  
Biological Effects ◽  
Vegf Receptor ◽  
Mesenchymal Transition ◽  
Cancer Management ◽  
Metabolic Role

The mevalonate pathway (also known as the cholesterol biosynthesis pathway) plays a crucial metabolic role in normal cell function as well as in the pathological environment. It leads to the synthesis of sterol and non-sterol isoprenoid biomolecules which subserve a variety of cellular functions. It is known to be deregulated in many disease processes. Statins and bisphosphonates are prominent inhibitors of the mevalonate pathway. They inhibit cell proliferation and activate apoptotic signalling and suppress tumour growth. Statins subdue metastatic spread of tumours by virtue of their ability to suppress invasion and angiogenesis. The induction of autophagy is another feature of statin effects that could contribute to the suppression of metastasis. Herein highlighted are the major signalling systems that statins engage to generate these biological effects. Statins can constrain tumour growth by influencing the expression and function of growth factor and receptor systems. They may suppress epithelial mesenchymal transition with resultant inhibition of cell survival signalling, together with the inhibition of cancer stem cell generation, and their maintenance and expansion. They can suppress ER (oestrogen receptor)-α in breast cancer cells. Statins have been implicated in the activation of the serine/threonine protein kinase AMPK (5&#039; adenosine monophosphate-activated protein) leading to the suppression of cell proliferation. Both statins and bisphosphonates can suppress angiogenic signalling by HIF (hypoxia- inducible factor)-1/eNOS (endothelial nitric oxide synthase) and VEGF (vascular endothelial growth factor)/VEGFR (VEGF receptor). Statins have been linked with improvements in disease prognosis. Also attributed to them is the ability of cancer prevention and reduction of risk of some forms of cancer. The wide spectrum of cancer associated events which these mevalonate inhibitors appear to influence would suggest a conceivable role for them in cancer management. However, much deliberation is warranted in the design and planning of clinical trials, their scope and definition of endpoints, modes risk assessment and the accrual of benefits.

Lentiviral-Mediated Overexpression of MicroRNA-141 Promotes Cell Proliferation and Inhibits Apoptosis in Human Esophageal Squamous Cell Carcinoma

2019 ◽  
Vol 14 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Jun-He Zhang ◽  
Hai-Bin Xia
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumour Growth ◽  
Direct Interaction ◽  
Vital Role ◽  
Expression Level ◽  
Luciferase Reporter

Background:Esophageal Carcinoma (EC) is the eighth most common cancer worldwide. Numerous studies have highlighted a vital role of microRNAs (miRNAs) in the development of EC. However, the mechanism of microRNA (miRNA)-141 in Esophageal Squamous Cell Carcinoma (ESCC) remains unknown.Objective:In this study, we explored the effects of miRNA-141 on EC cell proliferation, apoptosis, xenograft tumour growth and their possible mechanisms.Methods :A lentivirus-vector-expressing miRNA-141 was constructed, and a TE-1 cell line of ESCC with a stable expression of miRNA-141 was transfected and screened. The miRNA-141 expression level was detected using qRT-PCR. Effects of miRNA-141 overexpression on cell proliferation and apoptosis were detected using MTT and flow cytometry, respectively. Using a dual-luciferase reporter assay, a direct interaction between miRNA-141 and the 3'-Untranslated Region (UTR) of YAP1 and SOX17 was confirmed. Tumour xenograft experiment in nude mice was used to detect the tumour growth, and the effects of miRNA-141 overexpression on YAP1 and SOX17 were analysed using Western blot.Results:We found that miRNA-141 was highly expressed in TE-1 cells, and miRNA-141 overexpression promoted cell proliferation and inhibited apoptosis. Moreover, the miRNA-141 group showed significantly increased tumour growth ability, luciferase activities and expression levels of YAP1 and SOX17 in the miRNA-141group were significantly down-regulated.Conclusion:miRNA-141 promotes cell proliferation and inhibits apoptosis in ESCC by downregulating the expression level of YAP1 and SOX17, indicating that miRNA-141 may be a potential molecular target for the treatment of ESCC.

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