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Carvacrol protects human cervical cancer cells against cisplatin- induced cytotoxicity through multiple ERK-dependent mechanisms


Potočnjak, Iva; Gobin, Ivana; Domitrović, Robert
Carvacrol protects human cervical cancer cells against cisplatin- induced cytotoxicity through multiple ERK-dependent mechanisms // Book of Abstracts
Poreč, Hrvatska, 2017. str. 202-202 (poster, međunarodna recenzija, sažetak, znanstveni)


Naslov
Carvacrol protects human cervical cancer cells against cisplatin- induced cytotoxicity through multiple ERK-dependent mechanisms
(Carvacrol protects human cervical cancer cells against cisplatin-induced cytotoxicity through multiple ERK-dependent mechanisms)

Autori
Potočnjak, Iva ; Gobin, Ivana ; Domitrović, Robert

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Book of Abstracts / - , 2017, 202-202

Skup
25th Croatian Meeting of Chemists and Chemical Engineers with international participation, 3rd symposium “Vladimir Prelog”

Mjesto i datum
Poreč, Hrvatska, 19-22.04.2017

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
HeLa cells ; cisplatin ; carvacrol ; ERK MAPK ; apoptosis ; autophagy

Sažetak
Carvacrol, a natural compound, has been shown to possess anticancer activity. We investigated ERK MAPK signaling as a possible mechanism of cytotoxic activity of carvacrol against HeLa cervical cancer cells and occurrence of a drug−phytochemical interaction between cisplatin (CP) and carvacrol. HeLa cells were treated with carvarcol (550 μM) or CP (20 μM), alone or combined, without or with addition of the MEK inhibitor PD325901 (150 μM). Both carvacrol and CP activated ERK and showed cytotoxicity against HeLa cells. However, PD325901 increased cytotoxicity in carvacrol- treated cells, but increased survival of CP- treated cell. Co-treatment with carvacrol and CP increased HeLa cell survival compared to CP treatment, while MEK inhibition further increased their survival. The cell survival was negatively associated by the expression of Bax, cleaved caspase-9 and cleaved PARP. Co- treatment with CP and carvacrol suppressed apoptosis compared to CP-treated cells, while MEK inhibition resulted in further decrease in apoptosis. Additionally, carvacrol increased CP-induced expression of autophagy protein LC3B-II but not Beclin 1, which was enhanced by PD325901 treatment, suggesting ERK-dependent mechanism of autophagy. Nevertheless, other ERK-dependent and independent pathways were involved in cytoprotective activity of carvacrol, including IκBα/NF-κB and Akt/mTOR, depending on the type of the treatment. The results of the current study suggest that both carvacrol and CP showed cytotoxicity against HeLa cells, with the opposite role of ERK in the two treatments. In addition, carvacrol induced CP resistance in HeLa cells through ERK-mediated induction of autophagy and inhibition of apoptosis.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija



POVEZANOST RADA


Ustanove
Medicinski fakultet, Rijeka