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Pregled bibliografske jedinice broj: 918181

Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation


Potočnjak, Iva; Gobin, Ivana; Domitrović, Robert
Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation // Phytotherapy research, 32 (2018), 6; 1090-1097 (međunarodna recenzija, članak, znanstveni)


Naslov
Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation

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

Izvornik
Phytotherapy research (0951-418X) 32 (2018), 6; 1090-1097

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Cisplatin ; carvacrol ; HeLa cells ; MAPK ; apoptosis ; autophagy

Sažetak
Carvacrol has been shown to possess anticancer activity but the mechanism is unknown, as well as the possibility of interaction with anticancer drugs. The aim of this study was to investigate the role of mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling in carvacrol-induced human cervical cancer HeLa cell cytotoxicity. In addition, we studied sensitization of HeLa cells to cisplatin (CP) by carvacrol. Both carvacrol and CP showed dose-dependent cytotoxicity against HeLa cells and activated ERK1/2. The MEK inhibitor PD325901 suppressed ERK expression and further increased cytotoxicity of carvacrol but increased viability of CP-treated cells by modulating apoptosis. The MEK inhibitor also increased microtubule-associated protein 1A/1B- light chain 3 (LC3B) expression in CP treatment. Co-treatment with CP and carvacrol resulted in increased viability of the cancer cells compared to CP treatment, which was associated with the suppression of apoptosis. MEK inhibition decreased the cell viability, without changes in apoptosis. Concomitantly, carvacrol increased CP-induced expression of LC3B, which was enhanced by MEK inhibition. The results of the current study suggest the opposite role of ERK1/2 in carvacrol and CP- induced HeLa cell cytotoxicity. Interestingly, carvacrol induced CP resistance in HeLa cells through ERK1/2-independent suppression of apoptosis and ERK1/2-dependent modulation of autophagy.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija



POVEZANOST RADA


Ustanove
Medicinski fakultet, Rijeka

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE