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软骨寡聚基质蛋白通过增强侵袭和破坏细胞内钙稳态促进前列腺癌进展。

Cartilage oligomeric matrix protein promotes prostate cancer progression by enhancing invasion and disrupting intracellular calcium homeostasis.

作者信息

Englund Emelie, Canesin Giacomo, Papadakos Konstantinos S, Vishnu Neelanjan, Persson Emma, Reitsma Bart, Anand Aseem, Jacobsson Laila, Helczynski Leszek, Mulder Hindrik, Bjartell Anders, Blom Anna M

机构信息

Department of Translational Medicine, Division of Medical Protein Chemistry, Lund University, Malmö, Sweden.

Department of Translational Medicine, Division of Urological Cancers, Lund University, Malmö, Sweden.

出版信息

Oncotarget. 2017 Sep 21;8(58):98298-98311. doi: 10.18632/oncotarget.21176. eCollection 2017 Nov 17.

DOI:10.18632/oncotarget.21176
PMID:29228690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5716730/
Abstract

Cartilage oligomeric matrix protein (COMP) was recently implicated in the progression of breast cancer. Immunostaining of 342 prostate cancer specimens in tissue microarrays showed that COMP expression is not breast cancer-specific but also occurs in prostate cancer. The expression of COMP in prostate cancer cells correlated with a more aggressive disease with faster recurrence. Subcutaneous xenografts in immunodeficient mice showed that the prostate cancer cell line DU145 overexpressing COMP formed larger tumors as compared to mock-transfected cells. Purified COMP bound to and enhanced the invasion of DU145 cells in an integrin-dependent manner. In addition, intracellular COMP expression interfered with cellular metabolism by causing a decreased level of oxidative phosphorylation with a concurrent upregulation of lactate production (Warburg effect). Further, expression of COMP protected cells from induction of apoptosis via several pathways. The effect of COMP on metabolism and apoptosis induction was dependent on the ability of COMP to disrupt intracellular Ca signalling by preventing Ca release from the endoplasmic reticulum. In conclusion, COMP is a potent driver of the progression of prostate cancer, acting in an anti-apoptotic fashion by interfering with the Ca homeostasis of cancer cells.

摘要

软骨寡聚基质蛋白（COMP）最近被认为与乳腺癌的进展有关。对组织芯片中342例前列腺癌标本进行免疫染色显示，COMP表达并非乳腺癌所特有，在前列腺癌中也会出现。COMP在前列腺癌细胞中的表达与侵袭性更强、复发更快的疾病相关。免疫缺陷小鼠皮下异种移植显示，与mock转染细胞相比，过表达COMP的前列腺癌细胞系DU145形成的肿瘤更大。纯化的COMP以整合素依赖的方式结合并增强DU145细胞的侵袭能力。此外，细胞内COMP表达通过导致氧化磷酸化水平降低并同时上调乳酸生成（瓦伯格效应）来干扰细胞代谢。此外，COMP的表达通过多种途径保护细胞免受凋亡诱导。COMP对代谢和凋亡诱导的作用取决于COMP通过阻止内质网释放Ca来破坏细胞内Ca信号的能力。总之，COMP是前列腺癌进展的有力驱动因素，通过干扰癌细胞的Ca稳态以抗凋亡方式发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/c968ed283adb/oncotarget-08-98298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/3a59c5da0332/oncotarget-08-98298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/9c5a2f6b953b/oncotarget-08-98298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/d8139cf30202/oncotarget-08-98298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/8e501c490e63/oncotarget-08-98298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/08a6160b5d4e/oncotarget-08-98298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/c968ed283adb/oncotarget-08-98298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/3a59c5da0332/oncotarget-08-98298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/9c5a2f6b953b/oncotarget-08-98298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/d8139cf30202/oncotarget-08-98298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/8e501c490e63/oncotarget-08-98298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/08a6160b5d4e/oncotarget-08-98298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9809/5716730/c968ed283adb/oncotarget-08-98298-g006.jpg

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