Object

Title: The role of AMP-activated kinase (AMPK) in the regulation of the process of cancer cells metastasis

Abstract:

Cervical cancer (CC) is the fourth most common malignant cancer among women. Research of mechanisms leading to cancer progression is a hope for the discovery of new therapeutic goals. One of the promising areas of research is the metabolic context and the enzyme AMPK activated kinase. The aim of this dissertation was to investigate the role of AMPK kinase in the regulation of neoplastic cell metastasis in cervical cancer. Since the epithelial mesenchymal transition (EMT) is one of the mechanisms enabling cancer cell metastasis, cell lines, which molecularly well represent this process, have been used as a research model. In the cell lines used, genetic modifications were made that changed the expression of the AMPK kinase catalytic subunit α. CC lines were incubated with factors related to EMT induction and with pharmacological AMPK activators. It was shown that tumor progression leads to metabolic deregulation which is the phenomenon of silencing the expression and activity of AMPK. It has also been demonstrated that AMPK kinase is related to the ability of cells to acquire invasive phenotype in EMT and to the potential for in vivo metastases, and its activity may inhibit these processes. In conclusion, AMPK kinase may be a promising therapeutic target and the introduction of AMPK activators into anti-cancer therapy may help in the effective treatment of cancer.

Place of publishing:

Kraków

Level of degree:

2 - studia doktoranckie

Degree discipline:

onkologia ; ginekologia ; biochemia

Degree grantor:

Rada Dyscypliny Nauki medyczne

Promoter:

Majka, Marcin

Date issued:

2019

Identifier:

oai:dl.cm-uj.krakow.pl:4488

Call number:

ZB-132970

Language:

pol

Access rights:

nieograniczony

Object collections:

Last modified:

Dec 18, 2024

In our library since:

Feb 7, 2022

Number of object content hits:

115

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0

All available object's versions:

http://dl.cm-uj.krakow.pl:8080/publication/4489

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ZB-132970 Dec 18, 2024
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