Güngül, Taha Buğra

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https://hdl.handle.net/11147/16331
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Main Affiliation
01. Izmir Institute of Technology
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Current Staff
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Sustainable Development Goals

NO POVERTY1
NO POVERTY
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ZERO HUNGER2
ZERO HUNGER
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
1
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QUALITY EDUCATION4
QUALITY EDUCATION
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GENDER EQUALITY5
GENDER EQUALITY
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
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DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
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INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
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REDUCED INEQUALITIES10
REDUCED INEQUALITIES
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
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CLIMATE ACTION13
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LIFE BELOW WATER14
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LIFE ON LAND15
LIFE ON LAND
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PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
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PARTNERSHIPS FOR THE GOALS17
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Scholarly Output

1

Articles

1

Views / Downloads

5479/62

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

7

Scopus Citation Count

7

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WoS Citations per Publication

7.00

Scopus Citations per Publication

7.00

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0

Supervised Theses

0

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Journal of Cell Communication and Signaling1
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  • Article
    Citation - WoS: 7
    Citation - Scopus: 7
    Connexin 32 Overexpression Increases Proliferation, Reduces Gap Junctional Intercellular Communication, Motility and Epithelial-To Transition in Hs578t Breast Cancer Cells
    (Springer, 2022) Güngül, Taha Buğra; Meşe Özçivici, Gülistan; Uğur, Deniz; Özçivici, Engin; Yalçın Özuysal, Özden; Yücel, Simge; 03.01. Department of Bioengineering; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 03. Faculty of Engineering; 04. Faculty of Science
    Connexins (Cx) are primary components of gap junctions that selectively allow molecules to be exchanged between adjacent cells, regulating multiple cellular functions. Along with their channel forming functions, connexins play a variety of roles in different stages of tumorigenesis and their roles in tumor initiation and progression is isoform- and tissue-specific. While Cx26 and Cx43 were downregulated during breast tumorigenesis, Cx32 was accumulated in the cytoplasm of the cells in lymph node metastasis of breast cancers and Cx32 was further upregulated in metastasis. Cx32's effect on cell proliferation, gap junctional communication, hemichannel activity, cellular motility and epithelial-to-mesenchymal transition (EMT) were investigated by overexpressing Cx32 in Hs578T and MCF7 breast cancer cells. Additionally, the expression and localization of Cx26 and Cx43 upon Cx32 overexpression were examined by Western blot and immunostaining experiments, respectively. We observed that MCF7 cells had endogenous Cx32 while Hs578T cells did not and when Cx32 was overexpressed in these cells, it caused a significant increase in the percentages of Hs578T cells at the S phase in addition to increasing their proliferation. Further, while Cx32 overexpression did not induce hemichannel activity in either cell, it decreased gap junctional communication between Hs578T cells. Additionally, Cx32 was mainly observed in the cytoplasm in both cells, where it did not form gap junction plaques but Cx32 overexpression reduced Cx43 levels without affecting Cx26. Moreover, migration and invasion potentials of Hs578T and migration in MCF7 were reduced upon Cx32 overexpression. Finally, the protein level of mesenchymal marker N-cadherin decreased while epithelial marker ZO-1 and E-cadherin increased in Hs578T cells. We observed that Cx32 overexpression altered cell proliferation, communication, migration and EMT in Hs578T, suggesting a tumor suppressor role in these cells while it had minor effects on MCF7 cells.