PMID- 29717026
OWN - NLM
STAT- MEDLINE
DCOM- 20190308
LR  - 20190308
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 38
IP  - 3
DP  - 2018 Jun 29
TI  - Steroid receptor coactivator-1 interacts with NF-kappaB to increase VEGFC levels in 
      human thyroid cancer.
LID - BSR20180394 [pii]
LID - 10.1042/BSR20180394 [doi]
AB  - Thyroid cancer is the most common endocrine cancer, and has a high incidence of 
      lymphatic metastasis. Vascular endothelial growth factor C (VEGFC) is essential 
      for development of lymphatic vessels and lymphatic metastases during 
      carcinogenesis. Steroid receptor coactivator-1 (SRC-1) interacts with nuclear 
      receptors and transcription factors to promote tumor proliferation and 
      metastasis. However, the correlation between SRC-1 and VEGFC levels in the 
      lymphatic metastases of thyroid cancer remains unclear. We analyzed 20-paired 
      specimens of thyroid cancer tissue and normal thyroid tissue and found increased 
      levels of SRC-1 and VEGFC proteins in 13/20 and 15/20 thyroid cancer specimens, 
      respectively, when compared with those levels in specimens of normal thyroid 
      tissue. A high level of SRC-1 expression was positively correlated with VEGFC and 
      lymphatic endothelial cell marker LYVE-1 expression. Papillary thyroid carcinoma 
      cell line TPC-1 displayed high levels of SRC-1 and VEGFC expression and was 
      selected for stable knockdown of SRC-1 in vitro Inhibition of SRC-1 significantly 
      reduced the VEGFC levels in TPC-1 cells. We found that SRC-1 binds to 
      transcription factor NF-kB (p50/p65), and that this coactivation complex directly 
      promoted VEGFC transcription, which could be abrogated by SRC-1 knockdown. 
      Up-regulated NF-kB signaling was also confirmed in thyroid cancer tissues. In 
      vivo studies showed that SRC-1 knockdown restricted tumor growth, reduced the 
      numbers of LYVE-1-positive lymphatic vessels, and decreased the levels of VEGFC 
      in tumor tissues. These results suggest a tumorigenic role for SRC-1 in thyroid 
      cancer via its ability to regulate VEGFC expression.
CI  - (c) 2018 The Author(s).
FAU - Gao, Bo
AU  - Gao B
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China.
FAU - Guo, Lingji
AU  - Guo L
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China.
FAU - Luo, Donglin
AU  - Luo D
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China.
FAU - Jiang, Yan
AU  - Jiang Y
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China.
FAU - Zhao, Jianjie
AU  - Zhao J
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China.
FAU - Mao, Chengyi
AU  - Mao C
AD  - Department of Pathology, Research Institute of Surgery of Daping Hospital, Army 
      Military Medical University, Chongqing 400042, China.
FAU - Xu, Yan
AU  - Xu Y
AD  - Department of Breast and Thyroid Surgery, Research Institute of Surgery of Daping 
      Hospital, Army Military Medical University, Chongqing 400042, China 
      xuyan1288@yeah.net.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180612
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (LYVE1 protein, human)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (VEGFC protein, human)
RN  - 0 (Vascular Endothelial Growth Factor C)
RN  - 0 (Vesicular Transport Proteins)
RN  - EC 2.3.1.48 (NCOA1 protein, human)
RN  - EC 2.3.1.48 (Nuclear Receptor Coactivator 1)
SB  - IM
MH  - Adenoma/genetics/metabolism/pathology
MH  - Animals
MH  - Carcinoma/genetics/metabolism/pathology
MH  - Carcinoma, Medullary/genetics/metabolism/pathology
MH  - Carcinoma, Papillary/*genetics/metabolism/pathology
MH  - Cell Line, Tumor
MH  - *Gene Expression Regulation, Neoplastic
MH  - Heterografts
MH  - Humans
MH  - Lymphatic Metastasis
MH  - Mice
MH  - Mice, Nude
MH  - NF-kappa B/*genetics/metabolism
MH  - Nuclear Receptor Coactivator 1/antagonists & inhibitors/*genetics/metabolism
MH  - Protein Binding
MH  - RNA, Small Interfering/genetics/metabolism
MH  - Signal Transduction
MH  - Thyroid Neoplasms/*genetics/metabolism/pathology
MH  - Vascular Endothelial Growth Factor C/*genetics/metabolism
MH  - Vesicular Transport Proteins/genetics/metabolism
PMC - PMC5997793
OTO - NOTNLM
OT  - SRC-1
OT  - VEGFC
OT  - lymphatic metastases
OT  - thyroid cancer
COIS- The author declares that there are no competing interests associated with the 
      manuscript.
EDAT- 2018/05/03 06:00
MHDA- 2019/03/09 06:00
PMCR- 2018/06/12
CRDT- 2018/05/03 06:00
PHST- 2018/03/15 00:00 [received]
PHST- 2018/04/24 00:00 [revised]
PHST- 2018/05/01 00:00 [accepted]
PHST- 2018/05/03 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
PHST- 2018/05/03 06:00 [entrez]
PHST- 2018/06/12 00:00 [pmc-release]
AID - BSR20180394 [pii]
AID - 10.1042/BSR20180394 [doi]
PST - epublish
SO  - Biosci Rep. 2018 Jun 12;38(3):BSR20180394. doi: 10.1042/BSR20180394. Print 2018 
      Jun 29.