Treatment with 20(S)-ginsenoside Rg3 reverses multidrug resistance in A549/DDP xenograft tumors
- Chao Liu
- Quan Gong
- Ting Chen
- Juan Lv
- Zhiping Feng
- Pengjie Liu
- Zhiyong Deng
Published online on: January 24, 2018
Copyright: © Liu et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Multidrug resistance (MDR) is an obstacle for cancer chemotherapy. It was reported that 20(S)-ginsenoside Rg3 (hereafter Rg3) was able to regulate MDR in mouse leukemia cells. The present study investigated the effect of Rg3 on the MDR of A549 lung cancer cells. A cell viability assay revealed that Rg3 treatment increased cisplatin (DDP) cytotoxicity in DDP resistant A549 cells (A549/DDP). Furthermore, Rg3 increases the antitumor effect of DDP on A549/DDP xenograft mice. The expression of MDR‑mediated proteins, including P‑glycoprotein (P‑gp), multidrug resistance‑associated protein (MPR1) and lung resistance protein 1 (LPR1), was detected in tumor tissue of A549/DDP xenograft mice. The results revealed that Rg3 treatment inhibited the expression of these MDR‑associated proteins. Additionally, technetium‑99m labeled hexakis-2-methoxyisobutylisonitrile (99mTc‑MIBI) single‑photon emission computed tomography was used to monitor the effect of Rg3 on cisplatin sensitivity of A549/DDP xenograft tumors. It was observed that uptake of 99mTc‑MIBI was increased by Rg3 treatment, which indicated that Rg3 is able to effectively enhance chemotherapy sensitivity of A549/DDP xenograft tumors. Taken together, these results revealed that Rg3 may be able to reverse MDR of lung cancer via the downregulation of P‑gp, MPR1 and LPR1.