• Türkçe
    • English
  • English 
    • Türkçe
    • English
  • Login
View Item 
  •   DSpace@AGÜ
  • Enstitüler
  • Sosyal Bilimler Enstitüsü
  • İşletme ve Ekonomi İçin Veri Bilimi Ana Bilim Dalı Tez Koleksiyonu
  • View Item
  •   DSpace@AGÜ
  • Enstitüler
  • Sosyal Bilimler Enstitüsü
  • İşletme ve Ekonomi İçin Veri Bilimi Ana Bilim Dalı Tez Koleksiyonu
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

The inhibition of autophagy and hedgehog pathway leads to a decrease in the proliferation of cholangiocarcinoma

Thumbnail

View/Open

Yüksek Lisans Tezi (2.128Mb)

Access

info:eu-repo/semantics/openAccess

Date

2019

Author

AKTAŞ, NİHAN

Metadata

Show full item record

Abstract

Cholangiocarcinoma (CCA) is the second most common liver cancer type. The median survival rate of CCA patients is really low. Aberrant signaling pathways such as PI3K/AKT/mTOR pathway could be main drivers in CCA pathogenesis. Hedgehog (Hh) pathway is also dysregulated in several carcinomas including CCA. It regulates and crosstalks with autophagy, which is a lysosomal degradation process. There is no study showing the crosstalk between Hh pathway and autophagy in the context of CCA. Since both autophagy and Hh pathways are dysregulated in CCA, better understanding of how they crosstalk with each other and contribute to CCA pathogenesis is important. Considering this crosstalk between Hh pathway and autophagy, we conducted a combination treatment comprising Hh and autophagy pathway inhibitors in EGI-1 and TFK-1 CCA cell lines. In our study, we firstly checked anti-proliferative effects of Hh pathway inhibitor, GANT61, and different autophagy blockers using MTT and Annexin V assay and cell cycle analysis. After determination of IC30 of GANT61 (15 uM), chloroquine (25 uM for TFK-1 and 50 uM for EGI-1), and nocodazole (0.2 uM for EGI-1 and 0.4 uM for TFK-1), we conducted combination experiments. When we inhibit Hh pathway with targeting different steps of autophagy, we observed that proliferation of both EGI-1 and TFK-1 cells decreased compared to single treatments. After that, we checked the expression of autophagy-related LC3B protein and Akt, a negative regulator of autophagy, using western blotting after single treatments and combinational treatments. Based on the change in LC3B and Akt expression, we also concluded that, inhibition of autophagy with Hh pathway either induce or inhibit autophagy depends on the administered treatments. This study highlights the importance of deciphering the exact mechanisms that control autophagy in CCA, thus leading to better treatment.

URI

https://hdl.handle.net/20.500.12573/329

Collections

  • İşletme ve Ekonomi İçin Veri Bilimi Ana Bilim Dalı Tez Koleksiyonu [37]



DSpace software copyright © 2002-2015  DuraSpace
Contact Us | Send Feedback
Theme by 
@mire NV
 

 




| Policy | Instruction | Guide | Contact |
Advanced Search

sherpa/romeo

Browse

All of DSpaceCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsTypeLanguageDepartmentCategoryPublisherAccess TypeInstitution AuthorThis CollectionBy Issue DateAuthorsTitlesSubjectsTypeLanguageDepartmentCategoryPublisherAccess TypeInstitution Author

My Account

LoginRegister

Statistics

View Google Analytics Statistics

DSpace software copyright © 2002-2015  DuraSpace
Contact Us | Send Feedback
Theme by 
@mire NV
 

 


|| Policy || Guide|| Instruction || Library || Abdullah Gül University || OAI-PMH ||

Abdullah Gül University, Kayseri, Turkey
If you find any errors in content, please contact:

Creative Commons License
Abdullah Gül University Institutional Repository is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 Unported License..

DSpace@AGÜ:


DSpace 6.2

tarafından İdeal DSpace hizmetleri çerçevesinde özelleştirilerek kurulmuştur.