Inhibition Of Proliferation By Somatostatin Analogs In Two Kinds Of Lung Cancer Cell Lines

Objective:To observe the inhibition effect of somatostatin analogs (SSTA) octreotide (OCT) on proliferation of two kinds of lung cancer cell lines (A549 and NCI-H446) in vitro. Then discuss the probable mechanism of SSTA's antiproliferative action, and the perspective therapy in the lung cancer in clinical.Methods: Lung cancer cell lines A549 and NCI-H446 were cultured in vitro. After treatment with various concentration OCT for 24 and 48 hours,the proliferation capacity of lung cancer lines cells(A549 and NC-H446 ) was observed by MTT. Cell cycle and apoptosis was detected by flow cytometry(FCM)after treatment of lung cancer cell lines with various concentration OCT 48 hours, The expression of SSTR subtype 1-5 mRNA was determined by reverse transcription polymerase chain reaction(RT-PCR)method in the two kinds of lung cancer cell lines.Results:1. The MTT results showed that OCT obviously suppressed the prolification of A549 and NCI-H446 cell lines(P<0.05). Additionly, the effect of inhibiting the prolification of A549 depended on the concentration of OCT and time of incubation.2. After being treated with different concentration of OCT for 48 h, the mitotic cycle of both A549 and NCI-H446 cells were ceased in G0/G1 phase(P<0.05), and OCT arrested the A549 cell cycle at G0/G1 in a dose-dependent manner(P<0.05).3. Flow cytometry assay showed that OCT could not induced A549 and NCI-H446 cells to undergo apoptosis(Pï¹¥0.05).4. A549 cell express all of the somatostatin receptor subtype SSTR-mRNA while not the SSTR-3mRNA. NCI-H446 cell express SSTR-1,2,5mRNA. SSTR-1,2,5 mRNA levels in A549 cells were higher than in NCI-H446 cells. Conclusion:1.OCT can effectively inhibit the proliferation of lung cancer cell A549 in a dose- dependent and time dependent manner in vitro, blocked the cell cycle in G0/G1 phase, but could not induce the apoptosis of A549.2. OCT can also inhibit the proliferation of NCI-H446 in vitro, ceased the cell cycle in G0/G1 phase, and could not induce the apoptosis of NCI-H446 either.3. We could propose that, the different inhibition effect of OCT to these two cancer cell lines, maybe association with the different SSTR subtype and the different density of SSTR in these two cancer lines .