Serum Neurotensin in Human Pancreatic Cancer

1996 ◽  
Vol 82 (6) ◽  
pp. 592-595 ◽  
Author(s):  
Tamara Meggiato ◽  
Chiara Ferrara ◽  
Giovanna Tessari ◽  
Mario Plebani ◽  
Massimo De Paoli ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Cancer Patients ◽  
Human Cancer ◽  
Stage Iv ◽  
Serum Levels ◽  
Human Pancreatic Cancer ◽  
Human Cancer Cells ◽  
Control Subjects

The role of neurotensin as a physiologic regulator of exocrine pancreatic secretion is known, but the hormone has only recently been recognized as important mitogen in vitro for human cancer cells. The aim of this study was to evaluate the variations of serum levels of neurotensin in pancreatic cancer. We studied 58 patients: 13 control subjects, 20 pancreatic cancer patients, 11 chronic pancreatitis patients, and 14 cases of extrapancreatic disease. No differences were found between serum values of neurotensin in pancreatic cancer and control subjects or extrapancreatic disease. Significantly higher values were detected in chronic pancreatitis than in pancreatic cancer patients ( P <0.04). In chronic pancreatitis patients, the serum levels of neurotensin were correlated with serum amylase ( r = 0.95, P <0.01). Lower levels of neurotensin were found in stage IV pancreatic cancer than in stages I-II ( t = 1.82, P <0.04) and in grade II than in grade I ( t = 2.21, P <0.02). Significant correlations were found between serum levels of neurotensin and two indices of nutrition: albumin ( r = 0.60, P <0.05) and the percentage reduction in body weight (Z = 2.20, P <0.02). No correlations were found between serum levels of the hormone and size of the neoplasm or the survival of patients. We can conclude that the serum variations of neurotensin do not seem to be related to the progression of human pancreatic cancer. The variation of serum levels of the hormone may be linked to a poor nutritional status of the patient.

Serum procarboxypeptidase A and carboxypeptidase A levels in pancreatıc disease

2011 ◽  
Vol 31 (5) ◽  
pp. 447-451 ◽  
Author(s):  
Ozgur Kemik ◽  
Ahu Sarbay Kemik ◽  
Aziz Sumer ◽  
Hüseyin Beğenik ◽  
Ahmet Cumhur Dülger ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Cancer Patients ◽  
Serum Levels ◽  
Pancreatic Disease ◽  
Control Group ◽  
Carboxypeptidase A ◽  
Control Groups ◽  
Serum Samples ◽  
Acute And Chronic Pancreatitis

Background and objectives: To determine the serum levels of procarboxypeptidase A (pro-CPA) and carboxypeptidase A (CPA) in patients with acute and chronic pancreatitis and pancreatic cancer. Materials and methods: Serum samples obtained from 96 patients with acute pancreatitis, 101 patients with chronic pancreatitis, 98 patients with pancreatic cancer and 96 control groups were assayed for biochemical parameters and serum pro-CPA and CPA. Results: Serum pro-CPA and CPA levels were significantly higher in acute and in chronic pancreatic cancer patients compared to control group ( p < 0.001). Pancreatic cancer patients had significantly higher serum pro-CPA and CPA levels when compared with acute and chronic pancreatitis cases ( p < 0.001). Conclusion: These data prove for increased pro-CPA and CPA levels as a biomarker for the diagnosis of pancreatitis and pancreatic cancer.

Wound Healing, Anti-pancreatic Cancer, and α-amylase Inhibitory Potentials of the Edible Mushroom, Metacordyceps neogunnii

2021 ◽  
pp. 5249-5253
Author(s):  
Abdu Ghalib ALKolaibe ◽  
Waill A. Elkhateeb ◽  
Marwa O. Elnahas ◽  
El-Manawaty M. ◽  
Deng CY ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Wound Healing ◽  
Methanolic Extract ◽  
Human Cancer ◽  
Edible Mushroom ◽  
Human Pancreatic Cancer ◽  
Similar Species ◽  
Pancreatic Cell ◽  
Wound Healing Effect

Metacordyceps neogunnii is an edible mushroom that has been previously known as Cordyceps gunnii. Recently, it has been proven that Metacordyceps neogunnii differs from similar species by having longer asci and wider ascospores and is phylogenetically distinct to related species. Few studies are available to describe bioactivities exerted by Metacordyceps neogunnii extracts which is insufficient to evaluate the potency of this mushroom. Therefore, the current work was conducted to evaluate the in vitro α-Amylase inhibitory ability, wound healing, and anti-human pancreatic cancer activities of Metacordyceps neogunnii 80% methanolic extract. M. neogunnii extract showed no effect on human cancer pancreatic cell line (Paca2). However, the same extract exhibited slight wound healing effect. On the other hand, M. neogunnii extract exhibited good α-amylase inhibitory activity that reached 69.3±0.78%, and IC50 of 32.38±4.0.

scholarly journals Expression of Sortilin in Pancreatic Carcinoma and Influence of Pancreatic Cancer Cells by Sortilin siRNA Knockdown

2021 ◽  
Author(s):  
Di Xu ◽  
Fan Yu ◽  
Shangqing Liu ◽  
Cai Rong
Keyword(s):  
Pancreatic Cancer ◽  
Logistic Regression ◽  
Regression Analysis ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Roc Curve ◽  
Univariate Analysis ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

Abstract BackgroundCurrently, there are few effective therapeutic options for pancreatic cancer patients. Sortilin is a member of vps10p receptor family，reported in many types of cancers. However, the underlying mechanism and prognostic value of sortilin in pancreatic cancer are still unclear. ObjectiveUnderstand the expression of sortilin in pancreatic cancer, and analyze its mechanism that affects the occurrence and development of pancreatic cancer. MethodsA tissue microarray of 115 pancreatic cancer metastases was analyzed by immunohistochemistry. All data were analyzed by univariate analysis and multivariate analysis. Multivariate logistic regression analysis and the area under the receiver operating characteristic (ROC) curve were used to analyze the ability of sortilin in predicting pancreatic cancer. Next, survival analysis was performed to compare the survival time between high-risk and low-risk patients to validate the prognosis prediction efficacy of sortilin. The effects of sortilin on the invasion，metastasis and proliferation of pancreatic cancer cells were investigated both in vitro. investigate the anti-cancer effect of soritlin on human pancreatic cancer Capna1 and Bxpc3 cells, and its possible molecular mechanism. ResultsDifferential expression analysis of 115 tissue microarrays showed sortilin expression was up‐regulated in pancreatic cancer tissues,and it mainly comes from the nucleus. Sortilin expression in nucleus(SEIN) was only negatively correlated with N stage, Binary logistic regression model showed that SEIN is a good diagnostic marker for predicting pancreatic cancer and the accuracy of prediction is as high as 79.1 %. ROC curve analysis demonstrated a statistically significant diagnostic value of SEIN,and the diagnostic accuracy was 86.3%, The Youden Index was calculated to evaluate the diagnostic power, The cut-off value for SEIN in pancreatic cancer diagnosis was 0.85, with a sensitivity of 90.9% and a specificity of 68.3%. Univariate analysis showed that M stage(P=0.022), histological grade(P=0.021), clinic stage(P=0.030)and SEIN(P=0.039) were correlated with prognosis of pancreatic cancer patients, Multivariate regression analysis showed that M stage(P=0.036)and ESIN(P=0.004) were independent factors.The proliferation, invasion and migration of pancreatic cancer cells were inhibited in vitro by sortilin siRNA knockdown.it may have something to do with soritlin/P53/NFκB regulated the the proliferation function and sortilin/MMP9 regulated the invasion-promotion of pancreatic cancer cells. ConclusionsThese fndings demonstrated that the low expression of SEIN indicates better prognosis in pancreatic cancer and supplemented the effect mechanism of sortilin on pancreatic cancer cells. SEIN expression may serve as a potential diagnostic indicator of pancreatic cancer.

scholarly journals Restriction of extracellular lipids renders pancreatic cancer dependent on autophagy

2022 ◽  
Vol 41 (1) ◽  
Author(s):  
Maria Saliakoura ◽  
Matteo Rossi Sebastiano ◽  
Ioanna Nikdima ◽  
Chiara Pozzato ◽  
Georgia Konstantinidou
Keyword(s):  
Pancreatic Cancer ◽  
Fatty Acids ◽  
Cancer Cell ◽  
Human Cancer ◽  
Human Pancreatic Cancer ◽  
Ductal Adenocarcinoma ◽  
Extracellular Lipid ◽  
Autophagy Inhibition

Abstract Background KRAS is the predominant oncogene mutated in pancreatic ductal adenocarcinoma (PDAC), the fourth cause of cancer-related deaths worldwide. Mutant KRAS-driven tumors are metabolically programmed to support their growth and survival, which can be used to identify metabolic vulnerabilities. In the present study, we aimed to understand the role of extracellularly derived fatty acids in KRAS-driven pancreatic cancer. Methods To assess the dependence of PDAC cells on extracellular fatty acids we employed delipidated serum or RNAi-mediated suppression of ACSL3 (to inhibit the activation and cellular retention of extracellular fatty acids) followed by cell proliferation assays, qPCR, apoptosis assays, immunoblots and fluorescence microscopy experiments. To assess autophagy in vivo, we employed the KrasG12D/+;p53flox/flox;Pdx1-CreERT2 (KPC) mice crossed with Acsl3 knockout mice, and to assess the efficacy of the combination therapy of ACSL3 and autophagy inhibition we used xenografted human cancer cell-derived tumors in immunocompromised mice. Results Here we show that depletion of extracellularly derived lipids either by serum lipid restriction or suppression of ACSL3, triggers autophagy, a process that protects PDAC cells from the reduction of bioenergetic intermediates. Combined extracellular lipid deprivation and autophagy inhibition exhibits anti-proliferative and pro-apoptotic effects against PDAC cell lines in vitro and promotes suppression of xenografted human pancreatic cancer cell-derived tumors in mice. Therefore, we propose lipid deprivation and autophagy blockade as a potential co-targeting strategy for PDAC treatment. Conclusions Our work unravels a central role of extracellular lipid supply in ensuring fatty acid provision in cancer cells, unmasking a previously unappreciated metabolic vulnerability of PDAC cells.

Structure-Reactivity Relationships on Substrates and Inhibitors of the Lysine Deacylase Sirtuin 2 from Schistosoma Mansoni (SmSirt2)

2019 ◽  
Author(s):  
Daria Monaldi ◽  
Dante Rotili ◽  
Julien Lancelot ◽  
Martin Marek ◽  
Nathalie Wössner ◽  
...  
Keyword(s):  
Schistosoma Mansoni ◽  
Human Cancer ◽  
Egg Laying ◽  
Human Cancer Cells ◽  
Parasite Survival ◽  
Survival And Reproduction ◽  
Emergence Of Resistance ◽  
First Time ◽  
Parasitic Life Cycle

The only drug for treatment of Schistosomiasis is Praziquantel, and the possible emergence of resistance makes research on novel therapeutic agents necessary. Targeting of Schistosoma mansoni epigenetic enzymes, which regulate the parasitic life cycle, emerged as promising approach. Due to the strong effects of human Sirtuin inhibitors on parasite survival and reproduction, Schistosoma sirtuins were postulated as therapeutic targets. In vitro testing of synthetic substrates of S. mansoni Sirtuin 2 (SmSirt2) and kinetic experiments on a myristoylated peptide demonstrated lysine long chain deacylation as an intrinsic SmSirt2 activity for the first time. Focused in vitro screening of the GSK Kinetobox library and structure-activity relationships (SAR) of identified hits, led to the first SmSirt2 inhibitors with activity in the low micromolar range. Several SmSirt2 inhibitors showed potency against both larval schistosomes (viability) and adult worms (pairing, egg laying) in culture without general toxicity to human cancer cells.<br>

In Vitro and In Vivo Antitumor Efficacy of Docetaxel and Sorafenib Combination in Human Pancreatic Cancer Cells

2010 ◽  
Vol 999 (999) ◽  
pp. 1-11
Author(s):  
P. Ulivi ◽  
C. Arienti ◽  
W. Zoli ◽  
M. Scarsella ◽  
S. Carloni ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Antitumor Efficacy ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

scholarly journals A New Smoothened Antagonist Bearing the Purine Scaffold Shows Antitumour Activity In Vitro and In Vivo

2021 ◽  
Vol 22 (16) ◽  
pp. 8372
Author(s):  
Ana María Zárate ◽  
Christian Espinosa-Bustos ◽  
Simón Guerrero ◽  
Angélica Fierro ◽  
Felipe Oyarzún-Ampuero ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Antitumour Activity ◽  
Anticancer Compounds ◽  
Human Cancer Cells ◽  
Cycle Arrest ◽  
Apoptosis Inducer ◽  
Purine Ring

The Smoothened (SMO) receptor is the most druggable target in the Hedgehog (HH) pathway for anticancer compounds. However, SMO antagonists such as vismodegib rapidly develop drug resistance. In this study, new SMO antagonists having the versatile purine ring as a scaffold were designed, synthesised, and biologically tested to provide an insight to their mechanism of action. Compound 4s was the most active and the best inhibitor of cell growth and selectively cytotoxic to cancer cells. 4s induced cell cycle arrest, apoptosis, a reduction in colony formation and downregulation of PTCH and GLI1 expression. BODIPY-cyclopamine displacement assays confirmed 4s is a SMO antagonist. In vivo, 4s strongly inhibited tumour relapse and metastasis of melanoma cells in mice. In vitro, 4s was more efficient than vismodegib to induce apoptosis in human cancer cells and that might be attributed to its dual ability to function as a SMO antagonist and apoptosis inducer.

Rhodium(i) N-heterocyclic carbene complexes: synthesis and cytotoxic properties

2021 ◽  
Vol 45 (11) ◽  
pp. 5176-5183
Author(s):  
Ichraf Slimani ◽  
Serap Şahin-Bölükbaşı ◽  
Mustafa Ulu ◽  
Enes Evren ◽  
Nevin Gürbüz ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Mtt Assay ◽  
Incubation Time ◽  
Human Cancer ◽  
Cytotoxic Activities ◽  
Carbene Complexes ◽  
Human Cancer Cells ◽  
Benzimidazolium Salts ◽  
Ht 29

A series of benzimidazolium salts and their [RhCl(NHC)(COD)] complexes were synthesized. All compounds were screened for in vitro cytotoxic activities against a panel of human cancer cells (HT-29 colon, Ishikawa endometrial, U-87 glioblastoma) using the MTT assay for 48 h incubation time.

scholarly journals Oncogene APOL1 promotes proliferation and inhibits apoptosis via activating NOTCH1 signaling pathway in pancreatic cancer

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Jiewei Lin ◽  
Zhiwei Xu ◽  
Junjie Xie ◽  
Xiaxing Deng ◽  
Lingxi Jiang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Density Lipoprotein ◽  
Human Pancreatic Cancer ◽  
Luciferase Reporter ◽  
Notch1 Signaling ◽  
In Vivo Experiments ◽  
Notch1 Signaling Pathway

AbstractAPOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell proliferation, cell cycle, and apoptosis was verified via functional in vitro and in vivo experiments. The results showed that knockdown of APOL1 significantly inhibited the proliferation and promoted apoptosis of pancreatic cancer. In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer.

Sign in / Sign up

Export Citation Format

Share Document