肾实质和肾肿瘤组织中前列腺素E的生理和病理水平。

Physiological and pathological levels of prostaglandin E in renal parenchyma and neoplastic renal tissue.

作者信息

Verratti Vittore, Brunetti Luigi, Ferrante Claudio, Orlando Giustino, Recinella Lucia, Chiavaroli Annalisa, Leone Sheila, Wang Run, Berardinelli Francesco

机构信息

Department of Psychological Sciences, Health and Territory, "G. d'Annunzio" University, Chieti-Pescara, via dei Vestini 31, Chieti, Italy.

Department of Pharmacy, "G. d'Annunzio" University, Chieti-Pescara, via dei Vestini 31, Chieti, Italy.

出版信息

Prostaglandins Other Lipid Mediat. 2019 Apr;141:11-13. doi: 10.1016/j.prostaglandins.2019.02.004. Epub 2019 Feb 10.

DOI:10.1016/j.prostaglandins.2019.02.004

PMID:30742910

Abstract

Prostaglandin (PG)E seems to promote tumor proliferation by regulating cell growth, inhibiting apoptosis, promoting angiogenesis, and suppressing host immune surveillance of cancer cells. The suppression of prostaglandins biosynthesis is thought to be the main molecular mechanism for non-steroidal anti-inflammatory drugs antineoplastic effect. Yet the relationship between PGE and human renal cell carcinoma remains unclear. The aim of our study is to evaluate the PGE content in human renal parenchyma and Renal Cell Carcinoma. The study was conducted on 20 consecutive patients undergoing radical nephrectomy for Renal Cell Carcinoma. In the normal renal parenchyma and in the neoplastic renal tissue the PGE level was 83.43 ± 5.89 pg/mg and 289.67 ± 22.2 pg/mg, respectively (P < 0.0001). There was no relationship between PGE content and Renal Cell Carcinoma dimension, Fuhrman grade, pathological-Tumor-Node and Metastasis (pTNM) stage and histological subtype. The PGE over-content in neoplastic renal tissue suggests a role of PGE in development and progression of renal carcinoma.

摘要

前列腺素（PG）E似乎通过调节细胞生长、抑制细胞凋亡、促进血管生成以及抑制宿主对癌细胞的免疫监视来促进肿瘤增殖。前列腺素生物合成的抑制被认为是非甾体抗炎药抗肿瘤作用的主要分子机制。然而，PGE与人类肾细胞癌之间的关系仍不清楚。我们研究的目的是评估人类肾实质和肾细胞癌中PGE的含量。该研究对20例连续接受肾细胞癌根治性肾切除术的患者进行。在正常肾实质和肿瘤性肾组织中，PGE水平分别为83.43±5.89 pg/mg和289.67±22.2 pg/mg（P<0.0001）。PGE含量与肾细胞癌的大小、富尔曼分级、病理肿瘤-淋巴结转移（pTNM）分期及组织学亚型之间均无相关性。肿瘤性肾组织中PGE含量过高表明PGE在肾癌的发生和发展中起作用。