Efe, Eda

Profile URL
https://hdl.handle.net/11147/15966
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Email Address
Main Affiliation
01. Izmir Institute of Technology
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Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
Research Products
ZERO HUNGER2
ZERO HUNGER
0
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
1
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QUALITY EDUCATION4
QUALITY EDUCATION
0
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GENDER EQUALITY5
GENDER EQUALITY
0
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
0
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
0
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DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
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INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
0
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REDUCED INEQUALITIES10
REDUCED INEQUALITIES
0
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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CLIMATE ACTION13
CLIMATE ACTION
0
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LIFE BELOW WATER14
LIFE BELOW WATER
0
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LIFE ON LAND15
LIFE ON LAND
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PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
0
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PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
0
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This researcher does not have a Scopus ID.
This researcher does not have a WoS ID.
No records found in other affiliations.
Scholarly Output

2

Articles

1

Views / Downloads

2125/728

Supervised MSc Theses

1

Supervised PhD Theses

0

WoS Citation Count

17

Scopus Citation Count

19

Patents

0

Projects

0

WoS Citations per Publication

8.50

Scopus Citations per Publication

9.50

Open Access Source

1

Supervised Theses

1

JournalCount
European Journal of Cell Biology1
Current Page: 1 / 1

Scopus Quartile Distribution

Competency Cloud

GCRIS Competency Cloud
Author of Publication: search.filters.isAuthorOfPublication.7cb83f65-19da-4481-8afe-e248ee636cb7

Scholarly Output Search Results

Now showing 1 - 2 of 2
  • Article
    Citation - WoS: 17
    Citation - Scopus: 19
    Pro-Metastatic Functions of Notch Signaling Is Mediated by Cyr61 in Breast Cells
    (Elsevier, 2020) Küçükköse, Cansu; Yalçın Özuysal, Özden; Efe, Eda; Doğan, Hülya; Günyüz, Zehra Elif; Fıratlıgil Yıldırır, Burcu; Fıratlıgil, Burcu; Efe, Eda; Doğan, Hülya; Yalçın Özuysal, Özden; İlhan, Mustafa; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science
    Metastasis is the main cause of cancer related deaths, and unfolding the molecular mechanisms underlying metastatic progression is critical for the development of novel therapeutic approaches. Notch is one of the key signaling pathways involved in breast tumorigenesis and metastasis. Notch activation induces pro-metastatic processes such as migration, invasion and epithelial to mesenchymal transition (EMT). However, molecular mediators working downstream of Notch in these processes are not fully elucidated. CYR61 is a secreted protein implicated in metastasis, and its inhibition by a monoclonal antibody suppresses metastasis in xenograft breast tumors, indicating the clinical importance of CYR61 targeting. Here, we aimed to investigate whether CYR61 works downstream of Notch in inducing pro-metastatic phenotypes in breast cells. We showed that CYR61 expression is positively regulated by Notch activity in breast cells. Notch1-induced migration, invasion and anchorage independent growth of a normal breast cell line, MCF10A, were abrogated by CYR61 silencing. Furthermore, upregulation of core EMT markers upon Notch1-activation was impaired in the absence of CYR61. However, reduced migration and invasion of highly metastatic cell line, MDA MB 231, cells upon Notch inhibition was not dependent on CYR61 downregulation. In conclusion, we showed that in normal breast cell line MCF10A, CYR61 is a mediator of Notch1-induced pro-metastatic phenotypes partly via induction of EMT. Our results imply CYR61 as a prominent therapeutic candidate for a subpopulation of breast tumors with high Notch activity.
  • Master Thesis
    Investigating the Effect of Human Sacm1l Gene in the P53 Wild Type Breast Epithelial Mcf10a and Breast Cancer Mcf7 Cells
    (01. Izmir Institute of Technology, 2021) Efe, Eda; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science
    p53, tumor suppressor protein, plays role in the regulation of many cellular processes. Thus, p53 activity is controlled by a series of mechanisms, one of which is a redox reaction. However, redox regulation of p53 is not well defined in the literature. As a candidate of antioxidant, Sac1 gene mutation resulted in decreased levels of human p53 protein in transformed yeast, but the human homolog of Sac1 (SACM1L) has not been studied yet. SACM1L is known to function as a phosphoinositide phosphatase, hydrolyzes PI4P in the Golgi and ER. Previous studies demonstrated SACM1L depletion in HeLa cells led to decreased viability and arrest at the G2/M phase. However, no data were found on the association between the SACM1L and either directly p53 or p53 mediated cellular processes. We aimed to investigate the role of SACM1L in p53 controlled cellular processes like cell cycle and apoptosis in p53 wild type (wt) breast epithelial cells MCF10A and breast cancer cells MCF7 in the presence or absence of SACM1L gene. We demonstrated that SACM1L knockout MCF7 cells were arrested in the G1 phase, and number of proliferating cells was reduced, whereas overexpression of SACM1L did not change the proliferation, and cell cycle. Further, the rate of apoptosis was increased in SACM1L overexpressing and knockout MCF10A and MCF7 cells, supported by the findings of transcriptional analysis for p53 target genes. In conclusion, the greatest effect of SACM1L was observed in the apoptosis, but the underlying mechanisms are still unclear and must be further studied.