Diprophylline inhibits non‑small cell lung cancer A549 cell proliferation and migration, and promotes apoptosis, by downregulating PI3K signaling pathway

Zhao,Hong‑Ying; Ren,Yun‑Hui; Ren,Xiu‑Bao; Wang,Yu

doi:10.3892/ol.2018.9678

Diprophylline inhibits non‑small cell lung cancer A549 cell proliferation and migration, and promotes apoptosis, by downregulating PI3K signaling pathway

Authors:
- Hong‑Ying Zhao
- Yun‑Hui Ren
- Xiu‑Bao Ren
- Yu Wang
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Affiliations: Department of Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China, Department of Oncology, Daqing Longnan Hospital, Daqing, Heilongjiang 163453, P.R. China, Department of Oncology, Xuzhou Cancer Hospital, Xuzhou, Jiangsu 221000, P.R. China
Published online on: November 8, 2018 https://doi.org/10.3892/ol.2018.9678
Pages: 857-862
Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Diprophylline (DPL) is identified as a methylxanthine (MX) derivative. A number of MX derivatives are reported to have anti‑tumor effects. However, it is not clear whether DPL has a therapeutic effect on non‑small cell lung cancer (NSCLC). The aim of the present study was to investigate the effects of DPL on NSCLC and to elucidate the potential underlying mechanism. A Cell Counting Kit‑8 assay was used to evaluate the potential effect of DPL on A549 cell proliferation. Transwell invasion and migration assays were performed to assess the effect of DPL on A549 cell migration and invasion. Furthermore, the percentage of apoptotic cells was detected by flow cytometric analysis, and proteins associated with apoptosis, including apoptosis regulator Bcl‑2, apoptosis regulator BAX and active caspase‑3, were examined by western blotting. Finally, the expression levels of molecules relevant to phosphoinositide 3‑kinase (PI3K) signaling were detected by western blot analysis. The present study demonstrated that DPL may significantly inhibit A549 cell proliferation, migration and invasion. Furthermore, treatment with DPL may significantly induce A549 cell apoptosis. Finally, the protein expression levels associated with the PI3K signaling pathway were significantly inhibited in A549 cells following treatment with DPL. In conclusion, DPL may inhibit the proliferation and migration of NSCLC by inactivating the PI3K signaling pathway, and DPL is a promising novel therapeutic drug for NSCLC.

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