Cytochrome C Oxidase Subunit 4 (COX4): A Potential Therapeutic Target for the Treatment of Medullary Thyroid Cancer. (Record no. 5637)

MARC details
000 -LEADER
fixed length control field 02717nam a22003737a 4500
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 201006s20202020 xxu||||| |||| 00| 0 eng d
022 ## - INTERNATIONAL STANDARD SERIAL NUMBER
International Standard Serial Number 2072-6694
024 ## - OTHER STANDARD IDENTIFIER
Standard number or code 10.3390/cancers12092548 [doi]
024 ## - OTHER STANDARD IDENTIFIER
Standard number or code cancers12092548 [pii]
040 ## - CATALOGING SOURCE
Original cataloging agency Ovid MEDLINE(R)
099 ## - LOCAL FREE-TEXT CALL NUMBER (OCLC)
PMID 32911610
245 ## - TITLE STATEMENT
Title Cytochrome C Oxidase Subunit 4 (COX4): A Potential Therapeutic Target for the Treatment of Medullary Thyroid Cancer.
251 ## - Source
Source Cancers. 12(9), 2020 Sep 08.
252 ## - Abbreviated Source
Abbreviated source Cancers (Basel). 12(9), 2020 Sep 08.
253 ## - Journal Name
Journal name Cancers
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Year 2020
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Manufacturer FY2021
265 ## - SOURCE FOR ACQUISITION/SUBSCRIPTION ADDRESS [OBSOLETE]
Publication status epublish
266 ## - Date added to catalog
Date added to catalog 2020-10-06
520 ## - SUMMARY, ETC.
Abstract The nuclear-encoded subunit 4 of cytochrome c oxidase (COX4) plays a role in regulation of oxidative phosphorylation and contributes to cancer progression. We sought to determine the role of COX4 in differentiated (DTC) and medullary (MTC) thyroid cancers. We examined the expression of COX4 in human thyroid tumors by immunostaining and used shRNA-mediated knockdown of COX4 to evaluate its functional contributions in thyroid cancer cell lines. In human thyroid tissue, the expression of COX4 was higher in cancers than in either normal thyroid (p = 0.0001) or adenomas (p = 0.001). The level of COX4 expression correlated with tumor size (p = 0.04) and lymph-node metastases (p = 0.024) in patients with MTCs. COX4 silencing had no effects on cell signaling activation and mitochondrial respiration in DTC cell lines (FTC133 and BCPAP). In MTC-derived TT cells, COX4 silencing inhibited p70S6K/pS6 and p-ERK signaling, and was associated with decreased oxygen consumption and ATP production. Treatment with potassium cyanide had minimal effects on FTC133 and BCPAP, but inhibited mitochondrial respiration and induced apoptosis in MTC-derived TT cells. Our data demonstrated that metastatic MTCs are characterized by increased expression of COX4, and MTC-derived TT cells are vulnerable to COX4 silencing. These data suggest that COX4 can be considered as a novel molecular target for the treatment of MTC.
546 ## - LANGUAGE NOTE
Language note English
650 ## - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element IN PROCESS -- NOT YET INDEXED
651 ## - SUBJECT ADDED ENTRY--GEOGRAPHIC NAME
Institution MedStar Health Research Institute
651 ## - SUBJECT ADDED ENTRY--GEOGRAPHIC NAME
Institution MedStar Washington Hospital Center
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Department Medicine/Endocrinology
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Medline publication type Journal Article
700 ## - ADDED ENTRY--PERSONAL NAME
Local Authors Bikas, Athanasios
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Local Authors Burman, Kenneth D
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Local Authors Wartofsky, Leonard
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Local Authors Ylli, Dorina
790 ## - Authors
All authors Bikas A, Burman K, Costello J, Jensen K, Klubo-Gwiezdzinska J, Mendonca-Torres MC, Patel A, Reynolds SM, Thakur S, Vasko V, Wartofsky L, Ylli D
856 ## - ELECTRONIC LOCATION AND ACCESS
DOI <a href="https://dx.doi.org/10.3390/cancers12092548">https://dx.doi.org/10.3390/cancers12092548</a>
Public note https://dx.doi.org/10.3390/cancers12092548
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Koha item type Journal Article
Item type description Article
Holdings
Withdrawn status Lost status Damaged status Not for loan Collection Home library Current library Date acquired Total Checkouts Full call number Barcode Date last seen Price effective from Koha item type
          MedStar Authors Catalog MedStar Authors Catalog 10/06/2020   32911610 32911610 10/06/2020 10/06/2020 Journal Article

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