Octreotide is the favorable alternative for cisplatin resistance reversal of ovarian cancer in vitro and in nude mice in vivo

Riferimento: 
Eur J Gynaecol Oncol. 2012;33(6):584-90.
Autori: 
Shen Y, Ren ML, Shi YH, Zhang YX, Cai YL.
Fonte: 
Eur J Gynaecol Oncol. 2012;33(6):584-90.
Anno: 
2012
Azione: 
Octreotide (OCT) potrebbe inibire la proliferazione del cancro ovarico e promuovere l'apoptosi, tramite i recettori della Somatostatina 2 (SSTR2), invertire la resistenza al cisplatino attraverso l'inibizione della Multidrug-resistenza associata proteina 2 (MRP2), del recettore del fattore di crescita dell'epidermide (EGFR) e perfino l'espressione del gene glutatione S-transferasi-pi (GST-pi).
Target: 
Octreotide/cancro ovarico.

ABSTRACT
This study aimed to observe the effects of octreotide (OCT) on cisplatin resistance reversal of cancer cells in vitro and in nude mice in vivo. MTT method and flow cytometry were used to investigate the effect of cisplatin, OCT or the combination of these two compounds on the proliferation and apoptosis of SKOV3-DDP cells. The size and weight of xenograft tumors from the nude mice model were measured. Real-time PCR was used to detect the mRNA expression of SSTR2, MDR1, MRP2, GST-pi and EGFR in SKOV3/DDP cells following the different treatment. At the concentration of 2.5-20 g/ml, OCT significantly reduced IC50 (p < 0.05) and promoted apoptosis (p < 0.05) of SKOV3-DDP cells' response to cisplatin. Unchanged expression was found in SSTR2 on the SKOV3/DDP cell in vitro after OCT treatment, but increased expression in vivo (p < 0.05). OCT increased GST-pi expression (p < 0.05) and reduced MRP2 and EGFR expression (p < 0.05) in a dose-dependent manner. The similar results were obtained in mice in vivo experiment, except the reduced expression of GST-pi. It is suggested that OCT could inhibit ovarian cancer proliferation and promote apoptosis, via the cell surface SSTR2, and reverse cisplatin resistance through inhibition of MRP2, EGFR, and even GST-pi expressions.