Fig. 5.

The trimeric aptamer inhibits growth of gastric cancer cells both in vitro and in animals. (A) N87 cells (10³ cells per well) were plated on 96-well plates, and 24 h later, monomeric (2-2 and PR) or trimeric aptamers [2-2(t) and PR(t)] at 10 μM were added. Subsequently, cells were incubated at 37 °C for 7 d, and the medium was refreshed every other day. Cell proliferation was determined by using a commercial kit. (B) CD-1 nude mice were inoculated with 5 × 10⁶ N87 cells. Once tumors became palpable, mice were treated i.p., once per week (for eight times) with the ErbB-2–specific mAb431 (160 μg per week), the trimeric, ErbB-2–specific aptamer 2–2(t) (40 μg per week) or with PR(t) (40 μg per week). Untreated tumor-bearing mice were similarly monitored; their rate of tumor growth was statistically indistinguishable from the rate displayed by the PR(t)-treated group. Shown are the results of one of three experiments. Data represent mean ± SEM of seven mice per group.