AI Article Synopsis
- Multidrug resistance (MDR) is a significant challenge in cancer treatment, and 20(S)-ginsenoside Rg3 (Rg3) has been shown to regulate MDR in mouse leukemia cells.
- In the study, Rg3 was found to enhance the effectiveness of the chemotherapy drug cisplatin (DDP) on DDP-resistant A549 lung cancer cells, both in vitro and in xenograft mouse models.
- The treatment with Rg3 reduced the levels of MDR-associated proteins (P-gp, MPR1, and LPR1) and improved the uptake of a imaging agent, indicating that Rg3 may help reverse MDR in lung cancer, enhancing chemotherapy sensitivity.
Article Abstract
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 (Tc-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 Tc-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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835854 | PMC |
| http://dx.doi.org/10.3892/ol.2018.7849 | DOI Listing |
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