magistrsko delo
Povzetek
Lipidne kapljice (LK) so dinamični organeli, ki hranijo maščobe in uravnavajo uporabo lipidov v celici. LK imajo pomembno vlogo pri odpornosti celic na različne oblike celičnega stresa. Njihova vloga pri zaščiti celic pred feroptozo, posebno obliko celične smrti, ki je odvisna od prisotnosti železa in lipidne peroksidacije, še ni popolnoma jasna. Cilj magistrskega dela je bil raziskati vlogo encimov diacilglicerol aciltransferaz (DGAT), ki so odgovorni za sintezo trigliceridov in s tem biogenezo LK, pri obrambi rakavih celic pred feroptozo. Na celičnem modelu raka dojke smo farmakološko sprožili proces feroptoze s spojinama RSL3 in erastin ter raziskali, kako sočasna inhibicija encimov DGAT1 in DGAT2 vpliva na tvorbo LK in celično smrt. Ugotovili smo, da inhibitorji encimov DGAT znižajo nivo LK v celicah in povečajo občutljivost celic na feroptozo. Z inhibicijo posameznih encimov DGAT smo ugotovili, da je predvsem DGAT1 pomemben za preživetje celic v pogojih feroptoze. Ob dodatku inhibitorja feroptoze ferostatina-1 smo potrdili, da spojini RSL3 in erastin sprožita to vrsto celične smrti, in odkrili, da ferostatin-1 poveča količino LK v celicah. Prav tako smo ugotovili, da dokozaheksaenojska kislina spodbudi kopičenje LK in poveča feroptotsko celično smrt, medtem ko dodatek mononenasičene oleinske kisline ni škodljiv za celice. Rezultati magistrskega dela bodo pripomogli k boljšemu razumevanju vloge LK pri uravnavanju občutljivosti rakavih celic na feroptozo.
Ključne besede
lipidne kapljice;feroptoza;lipidna peroksidacija;obrambni sistemi celic;magistrska dela;
Podatki
Jezik: |
Slovenski jezik |
Leto izida: |
2023 |
Tipologija: |
2.09 - Magistrsko delo |
Organizacija: |
UL FKKT - Fakulteta za kemijo in kemijsko tehnologijo |
Založnik: |
[S. Jereb] |
UDK: |
577.24:577.115:618.19-006(043.2) |
COBISS: |
174317059
|
Št. ogledov: |
68 |
Št. prenosov: |
10 |
Ocena: |
0 (0 glasov) |
Metapodatki: |
|
Ostali podatki
Sekundarni jezik: |
Angleški jezik |
Sekundarni naslov: |
The role of lipid droplets in the protection of breast cancer cells against ferroptosis |
Sekundarni povzetek: |
Lipid droplets (LDs) are dynamic fat storage organelles that control the use of lipids within cells. LDs play important roles in the cellular resilience against various forms of stress. However, their role in protecting cells against ferroptosis, a specific form of cell death dependent on iron and lipid peroxidation, is not yet fully understood. The aim of this master's thesis was to investigate the role of diacylglycerol acyltransferase (DGAT) enzymes, which are responsible for triglyceride synthesis and thus LD biogenesis, in the protection of cancer cells against ferroptosis. Using a breast cancer cell model, we induced ferroptosis using RSL3 and erastin and explored how combined inhibition of DGAT1 and DGAT2 affects LD formation and cell death. We found that inhibitors of DGAT enzymes decrease the level of LDs in cells and increase cell sensitivity to ferroptosis. By inhibiting individual DGAT enzymes, we determined that DGAT1 is important for cell survival under ferroptotic conditions. Using a ferroptosis inhibitor, ferrostatin-1, we confirmed that RSL3 and erastin trigger ferroptosis and discovered that ferrostatin-1 increases the amount of LDs in cells. Furthermore, we also found that docosahexaenoic acid promotes LD accumulation and increases ferroptotic cell death, while the addition of monounsaturated oleic acid is not detrimental to breast cancer cells. The findings of this master's thesis will contribute to a better understanding of the role of LDs in regulating the sensitivity of cancer cells to ferroptosis. |
Sekundarne ključne besede: |
lipid droplets;ferroptosis;lipid peroxidation;cell death;breast cancer;Lipidi;Celična smrt;Rak dojke;Univerzitetna in visokošolska dela; |
Vrsta dela (COBISS): |
Magistrsko delo/naloga |
Študijski program: |
1000377 |
Konec prepovedi (OpenAIRE): |
1970-01-01 |
Komentar na gradivo: |
Univ. v Ljubljani, Fak. za kemijo in kemijsko tehnologijo, smer Biokemija |
Strani: |
54 str. |
ID: |
20301375 |