東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Roles of epithelial-mesenchymal tran...

Uthaya Kumar, Dinesh Babu.

Linked to FindBook

Google Book

Amazon

博客來

Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells./
Author:	Uthaya Kumar, Dinesh Babu.
Description:	68 p.
Notes:	Source: Masters Abstracts International, Volume: 54-01.
Contained By:	Masters Abstracts International54-01(E).
Subject:	Pathology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1568207
ISBN:	9781321305012

Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells.
Uthaya Kumar, Dinesh Babu.

Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells. - 68 p.

Source: Masters Abstracts International, Volume: 54-01.

Thesis (M.S.)--University of Southern California, 2014.

This item is not available from ProQuest Dissertations & Theses.

BACKGROUND & AIMS: Alcohol and obesity cause steatohepatitis through activation of Toll-like receptor-4 (TLR4) signaling and enhance hepatitis C virus (HCV) associated liver carcinogenesis. The HCV NS5A protein ectopoically upregulates TLR4 in hepatocytes, generates TLR4/NANOG dependent liver tumor initiating stem cell-like cells (TICs), and induces liver tumor in alcohol fed transgenic (Tg) mice. These TICs have robust and selective expression of the leptin receptor, and increased phosphorylation and activation of STAT3. However, whether the TLR4-NANOG pathway promotes an oncogenic signaling in other etiological mouse models and patients is ambiguous. METHOD: We sought to determine whether a Western diet high in cholesterol, and saturated fat (HCFD) that causes obesity can also synergistically induce liver tumors via TLR4 signaling. RESULTS: We have identified the TLR4- NANOG oncogenic pathway in the genesis of TICs, and liver tumor in alcohol and/or HCFD fed NS5A Tg mice. An sensitized response in TICs to LPS and/or Leptin resulted in an enchanced Twist1 Promoter activity, which was abrogated by silencing: Tlr4, Nanog or Stat3. We provide evidence of NANOG and STAT3 sharing their binding site on Twist1 promoter to transactive it. CONCLUSION: Taken together, TLR4-NANOG axis promotes liver tumorigenesis/metastasis through accentuated mesenchymal phenotype with elevated Twist1 expression upon exposure to HCV and alcohol/high-fat diets. The TLR4 pathway serves as a novel therapeutic target for HCC.

ISBN: 9781321305012Subjects--Topical Terms:

643180
Pathology.

Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells.
LDR:02498nmm a2200301 4500 001 2064695
005 20151117142820.5
008 170521s2014 ||||||||||||||||| ||eng d
020 $a 9781321305012
035 $a (MiAaPQ)AAI1568207
035 $a AAI1568207
040 $a MiAaPQ $c MiAaPQ
100 1 $a Uthaya Kumar, Dinesh Babu. $3 3179315
245 1 0 $a Roles of epithelial-mesenchymal transition and niche in tumorigenesis of tumor-initiating cells.
300 $a 68 p.
500 $a Source: Masters Abstracts International, Volume: 54-01.
500 $a Adviser: Keigo Machida.
502 $a Thesis (M.S.)--University of Southern California, 2014.
506 $a This item is not available from ProQuest Dissertations & Theses.
520 $a BACKGROUND & AIMS: Alcohol and obesity cause steatohepatitis through activation of Toll-like receptor-4 (TLR4) signaling and enhance hepatitis C virus (HCV) associated liver carcinogenesis. The HCV NS5A protein ectopoically upregulates TLR4 in hepatocytes, generates TLR4/NANOG dependent liver tumor initiating stem cell-like cells (TICs), and induces liver tumor in alcohol fed transgenic (Tg) mice. These TICs have robust and selective expression of the leptin receptor, and increased phosphorylation and activation of STAT3. However, whether the TLR4-NANOG pathway promotes an oncogenic signaling in other etiological mouse models and patients is ambiguous. METHOD: We sought to determine whether a Western diet high in cholesterol, and saturated fat (HCFD) that causes obesity can also synergistically induce liver tumors via TLR4 signaling. RESULTS: We have identified the TLR4- NANOG oncogenic pathway in the genesis of TICs, and liver tumor in alcohol and/or HCFD fed NS5A Tg mice. An sensitized response in TICs to LPS and/or Leptin resulted in an enchanced Twist1 Promoter activity, which was abrogated by silencing: Tlr4, Nanog or Stat3. We provide evidence of NANOG and STAT3 sharing their binding site on Twist1 promoter to transactive it. CONCLUSION: Taken together, TLR4-NANOG axis promotes liver tumorigenesis/metastasis through accentuated mesenchymal phenotype with elevated Twist1 expression upon exposure to HCV and alcohol/high-fat diets. The TLR4 pathway serves as a novel therapeutic target for HCC.
590 $a School code: 0208.
650 4 $a Pathology. $3 643180
650 4 $a Immunology. $3 611031
650 4 $a Cellular biology. $3 3172791
690 $a 0571
690 $a 0982
690 $a 0379
710 2 $a University of Southern California. $b Molecular Microbiology & Immunology. $3 3179316
773 0 $t Masters Abstracts International $g 54-01(E).
790 $a 0208
791 $a M.S.
792 $a 2014
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1568207