George Emmanouil

University of Crete

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Moursellas Andrew

University of Crete

Argyro Voumvouraki

AHEPA University Hospital

M Tzardi

University Hospital of Heraklion

Elias Kouroumalis

University Hospital of Heraklion

ΜΓ

Μαρία Γεωργιάδου

University of Crete

Elias Kouroumalis

University of Crete

Georgios Ayiomamitis

Tzaneion General Hospital

George Notas

University of Crete

Ioannis Drygiannakis

University of Crete

Argyro Voumbouraki

AHEPA University Hospital

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University of Crete

University Hospital of Heraklion

California Liver Research Institute

AHEPA University Hospital

National and Kapodistrian University of Athens

Foundation for Research and Technology Hellas

FORTH Institute of Applied and Computational Mathematics

Tzaneion General Hospital

University Medical Center Hamburg-Eppendorf

Universität Hamburg

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Differential Effects of Somatostatin on TNF Receptors and Apoptosis in Hepatocellular Carcinoma Cell Lines

Gastroenterology Insights (2024)

Μαρία Γεωργιάδου George Notas Ioannis Tsomidis Argyro Voumbouraki Ioannis Drygiannakis

The anti-tumoral activity of somatostatin has been demonstrated in both animal experiments and human tumors. Clinical trials have reported conflicting results. We therefore hypothesized that somatostatin might have different effects in various hepatocellular carcinoma cells. Their clarification would possibly allow for the better selection of patients suitable for the optimal treatment results. We studied the mRNA and protein expression of TNF receptors and the TNFa-induced apoptosis using the HepG2 and the Hep3B human hepatocellular carcinoma cells after incubation with the somatostatin analog octreotide. RT-PCR, Western blot, and parameters associated with apoptosis (NF-kB nuclear translocation, P65 Ser536 and P65 Ser468 phosphorylation, DNA fragmentation) were assessed. Only TNFR1 was constitutively present in the two cell lines. Octreotide incubation led to an earlier reduction in TNFR1 mRNA and protein in HepG2 compared to Hep3B cells (1 h and 6–12 h, respectively). NF-kB translocation to the nucleus was induced by TNFa and was more prominent in Hep3B. Translocation was unaffected by octreotide. Serine phosphorylation was significantly induced by TNFa and was more evident in the Hep3B cells. TNFa-induced Ser536 phosphorylation was inhibited by octreotide only in the HepG2 cells. DNA fragmentation was not influenced by either octreotide or TNFa in the HepG2 cells, but TNFa induced fragmentation in the Hep3B cells (1.8-fold increase) verified by the TUNEL index (43 compared to 19 for the HepG2 cells). Octreotide and TNFa co-incubation induced apoptosis in the HepG2 cells (1.7-fold increase compared to controls) but inhibited apoptosis in the Hep3B cells. We conclude that: (1) octreotide reduced TNFR1 receptor expression in both cell lines, (2) parameters of apoptosis were differentially affected by octreotide in the two cell lines, and (3) this might be a partial explanation for the conflicting results of somatostatin analog treatment in human hepatocellular carcinoma trials.

Fragmentation

10.3390/gastroent15030045

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Angiodrastic Chemokines in Colorectal Cancer: Clinicopathological Correlations

Analytical Cellular Pathology (2018)

George Emmanouil Georgios Ayiomamitis Adamantia Zizi-Sermpetzoglou M Tzardi Moursellas Andrew

Aim . To study the expression of angiodrastic chemokines in colorectal tumors and correlate findings with clinicopathological parameters and survival. Methods . The proangiogenic factor VEGF, the angiogenic chemokines CXCL8 and CXCL6, and the angiostatic chemokine CXCL4 were measured by ELISA in tumor and normal tissue of 35 stage II and III patients and correlated with the histopathology markers Ki67, p53, p21, bcl2, EGFR, and MLH1 and 5-year survival. The Wilcoxon and chi-square tests were used for statistical comparisons. Results . There was a significant increase of CXCL6 (p=0.005) and VEGF (p=0.003) in cancerous tissue compared to normal. Patients with lower levels of CXCL8 and CXCL4 lived significantly longer. Patients with loss of EGFR expression had higher levels of CXCL8 while p21 loss was associated with higher levels of CXCL6. Chemokine levels were not correlated with TNM or Dukes classification. Strong expression of p53 was accompanied by decreased survival. Conclusions . (1) The angiogenic factors CXCL6 and VEGF are increased in colorectal cancer tissue with no association with the clinical stage of the disease or survival. (2) However, increased levels of tissue CXCL8 and CXCL4 are associated with poor survival. (3) Strong expression of p53 is found in patients with poor survival.

Interleukin 8

MLH1

10.1155/2018/1616973

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Angiodrastic Chemokines Production by Colonic Cancer Cell Lines

Onco (2022)

George Emmanouil Moursellas Andrew M Tzardi Argyro Voumvouraki Elias Kouroumalis

Purpose: To study the production of angiodrastic chemokines by colonic cancer cell lines. Methods: A pro-angiogenic factor (VEGF), two angiogenic chemokines (CXCL8, CXCL6), and one angiostatic (CXCL4) chemokine were measured by ELISA in the supernatants of the colon cancer cell lines HT-29 and Caco-2. Cells were cultured for 24 h in the presence of serum from cancer patients or healthy individuals. Results were analyzed by one-way ANOVA and the General Linear Model for repeated measures. Results: Colonic epithelial cells are potent producers of angiodrastic chemokines. HT-29 and Caco-2 cells produce all four chemokines under basal conditions and 24 h after incubation with human serum. The secretion response, however, was completely different. HT-29 cells produce more CXCL8 and VEGF irrespective of culture conditions, while Caco-2 cells seem unresponsive with respect to CXCL6 and CXCL4. Moreover, HT-29 cells produce more CXCL8 and VEGF when incubated with cancer serum, contrary to Caco-2 cells which produce more CXCL4 under the same conditions. Conclusions: The two colon cancer cell lines were producers of all chemokines studied, but their responses were not uniform under similar culture conditions. CXCL8 and VEGF are differently regulated compared to CXCL4 and CXCL6 in these two cell lines

Interleukin 8

10.3390/onco2020006

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