Related Experiment Video
Updated: Aug 17, 2026
In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration
Published on: February 23, 2019
Effect of arsenic trioxide on multidrug resistant hepatocellular carcinoma cells
Judy Yuet-Wa Chan1, Katy Pak-Yan Siu, Kwok-Pui Fung
1Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China.
Abstract:
Our previous study showed that arsenic trioxide (As2O3) was effective in inhibiting the growth of human hepatocellular carcinoma (HepG2) cells via induction of apoptosis. In the present study, we examined the effect of As2O3 on multidrug resistant human hepatocellular carcinoma (R-HepG2) cells which are characterized with overexpression of mdr1 gene and P-glycoprotein. The anti-proliferation of R-HepG2 by As2O3 was examined by MTT assay. For the induction of apoptosis, DNA fragmentation and Annexin V-PI staining were performed after treatment with arsenic trioxide. To study the effect of arsenic trioxide on P-glycoprotein, Western analysis probing anti-P-glycoprotein antibody was used to monitor the change of its expression. Results showed that As2O3 was effective in inhibiting the cell proliferation of R-HepG2 cells in a dose- and time-dependent manner via induction of apoptosis without affecting the cell cycle. The sensitivity of R-HepG2 cells toward As2O3 was found to be similar to that of the parental HepG2 cells. The Western analysis showed that As2O3 was probably not the substrate to be bound and extruded by P-glycoprotein in R-HepG2 cells because it could not maintain the cellular P-glycoprotein expression.
Insights
Arsenic trioxide effectively inhibits multidrug-resistant liver cancer cells by inducing apoptosis. This compound shows similar efficacy to parental cells, suggesting it is not affected by P-glycoprotein drug resistance mechanisms.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Hepatocellular carcinoma (HCC) is a major global health concern.
- Multidrug resistance (MDR) in HCC, often mediated by P-glycoprotein (P-gp), limits treatment efficacy.
- Arsenic trioxide (As2O3) has previously shown anti-cancer properties in HCC cells.
Purpose of the Study:
- To investigate the efficacy of As2O3 against multidrug-resistant HCC cells (R-HepG2).
- To determine if As2O3 induces apoptosis in R-HepG2 cells.
- To assess the interaction of As2O3 with P-glycoprotein in R-HepG2 cells.
Main Methods:
- Cell proliferation was assessed using MTT assay.
- Apoptosis was evaluated through DNA fragmentation and Annexin V-PI staining.
- P-glycoprotein expression was analyzed via Western blot.
Main Results:
- As2O3 inhibited R-HepG2 cell proliferation in a dose- and time-dependent manner.
- As2O3 induced apoptosis in R-HepG2 cells without affecting the cell cycle.
- R-HepG2 cells exhibited similar sensitivity to As2O3 as parental HepG2 cells.
- As2O3 did not appear to be a substrate for P-glycoprotein, as it did not affect P-gp expression.
Conclusions:
- As2O3 demonstrates significant anti-proliferative and apoptosis-inducing effects on multidrug-resistant liver cancer cells.
- The efficacy of As2O3 is not diminished by P-glycoprotein overexpression, suggesting a potential therapeutic role in resistant HCC.
- As2O3 may bypass common MDR mechanisms in HCC, offering a promising avenue for treatment.
Related Concept Videos
02:56Treatment Resistant Cancers
02:49Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...