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. 2020 Apr 27;12(5):1088. doi: 10.3390/cancers12051088

Figure 5.

Figure 5

Suppression of growth and progression in gastric cancer cells by the blockade of the mevalonate pathway is partially reversed by HMGCS1 overexpression. (A) For the blockade of the mevalonate pathway, AGS, KATO III, and NCI-N87 cells were treated with 2.5 or 5 μM lovastatin (statin) and/or dipyridamole (DP) for 24 h. Then, whole-cell extracts of the treated cells were prepared for Western blot analyses using anti-HMGCS1 and anti-GAPDH antibodies. (B–D) AGS, KATO III, and NCI-N87 cells were transfected with the HMGCS1-expressing construct (HMGCS1) or empty vector (EV) for 48 h. Then, the transfected cells were treated with lovastatin and/or dipyridamole for 24 h for the subsequent MTT assay (B). The transfected KATO III and NCI-N87 cells were also seeded for assays of tumorsphere formation (C), migration, invasion, and colony formation (D) in the presence or absence of 2.5 μM of lovastatin and/or dipyridamole. Mean ± SD (n = 3). *, P < 0.05; **, P < 0.01; ***, p < 0.001. #, p < 0.05; ##, p < 0.01; ###, p < 0.001.