ApolipoproteinL1 is expressed in papillary thyroid carcinomas

被引：18

作者：

Chidiac, Mounia ^{[1
,2
]}

Fayyad-Kazan, Mohammad ^{[1
]}

Daher, Jalil ^{[1
]}

Poelvoorde, Philippe ^{[1
]}

Bar, Isabelle ^{[3
]}

Maenhaut, Carine ^{[4
]}

Delree, Paul ^{[5
]}

Badran, Bassam ^{[2
]}

Vanhamme, Luc ^{[1
,6
]}

机构：

[1] Univ Libre Bruxelles, Inst Mol Biol & Med IBMM, Rue Prof Jeener & Brachet 12, B-6041 Gosselies, Belgium

[2] Lebanese Univ, Fac Sci, Dept Biochem, Immunol Lab, Beirut 21219, Lebanon

[3] Grand Hop Charleroi, Inst Pathol & Genet, Lab Translat Oncol, Ave Georges Lemaitre 25, B-6047 Gosselies, Belgium

[4] Univ Libre Bruxelles, Welbio, Inst Interdisciplinary Res IRIBHM, Route Lennik 808, B-1070 Brussels, Belgium

[5] Inst Pathol & Genet, Dept Pathol, Ave Georges Lemaitre 25, B-6041 Gosselies, Belgium

[6] Univ Libre Bruxelles, CHU Charleroi, A Vesale Hosp, Expt Med Lab,ULB Unit 222, Montignies le Tilleul, Belgium

来源：

PATHOLOGY RESEARCH AND PRACTICE | 2016年 / 212卷 / 07期

关键词：

Papillary thyroid carcinoma; Cancer; Apolipoprotein L1; LIPID-BINDING PROTEIN; AUTOPHAGIC CELL-DEATH; GENE-EXPRESSION; CANCER; BCL-2; OVEREXPRESSION; METASTASIS; PATHWAYS;

D O I：

10.1016/j.prp.2016.04.004

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

The apolipoprotein L (apoL) family has not yet been ascribed any definite patho-physiological function although the conserved BH3 protein domain suggests a role in programmed cell death. As repression of the regular apoptotic program is considered a hallmark of tumor progression, we investigated apoL expression in cancer. We show that the levels of one member of the family, apolipoprotein L1 (apoL1) is higher in papillary thyroid carcinoma compared to normal tissue. A combination of qRTPCR, immunohis-to-chemistiy and in situ hybridization allowed us to ascribe this increase to endogenous overexpression in carcinoma cells. Whether apoL1 plays an instrumental role in refraining cell death is the subject of ongoing molecular biology experiments. (C) 2016 Elsevier GmbH. All rights reserved.

引用

页码：631 / 635

页数：5

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