Phosphoinositide 3-kinase/Akt pathway is involved in pingyangmycin‑induced growth inhibition, apoptosis and reduction of invasive potential in EOMA mouse hemangioendothelioma cells.
Pingyangmycin (PYM), a glycopeptide antibiotic, has been recommended as a stand treatment for hemangioma. However, the underlying mechanisms of its anti‑tumor effects have remained elusive. The purpose of the present study was to explore the effects of PYM on the biological behavior of the EOMA mouse hemangioendothelioma cell line and investigate the possible mechanisms. The effects of PYM on EOMA cell viability were determined by an MTT assay, apoptosis was evaluated by Annexin V/propidium iodide staining and flow cytometric analysis, and cell invasion ability was determined using a Transwell invasion assay. In order to investigate the underlying mechanism of action of PYM, the expression of angiogenic signaling proteins was determined by western blot analysis. PYM treatment (0.5‑500 µg/ml) inhibited cell growth in a time- and dose‑dependent manner. PYM at 100 µg/ml significantly induced apoptosis and reduced the invasive ability of EOMA cells. Effects of PYM on cell viability, apoptosis and invasion ability were completely blocked by co‑treatment with phosphoinositide 3‑kinase (PI3K) activator insulin‑like growth factor‑1 (IGF‑1). Furthermore, treatment with PYM reduced the expression of PI3K and phosphorylated Akt. In conclusion, the present study indicated that the PI3K/Akt pathway is likely to be involved in the anti-cancer effects of PYM on EOMA cells.
Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Li-Xia
LX
Peng
Department of Breast Surgery, The Third Hospital Affiliated to Kunming Medical University, Kunming, Yunnan 650000, P.R. China.
Ping
P
Zhao
Department of General Surgery, The Second People's Hospital of Dehong, Dehong, Yunnan 678400, P.R. China.
Hong-Sheng
HS
Zhao
Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Er
E
Pan
Department of Dermatology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan 650000, P.R. China.
Bin-Bin
BB
Yang
Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Qin
Q
Li
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D001761:Bleomycin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D006390:Hemangioendothelioma / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D009361:Neoplasm Invasiveness / Q000235:genetics; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects
D000900:Anti-Bacterial Agents; D001761:Bleomycin; C025703:bleomycetin; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt