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Updated: Apr 24, 2026
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
ABCG2 regulates the pattern of self-renewing divisions in cisplatin-resistant non-small cell lung cancer cell lines
Ying Tang1, Jingming Hou2, Guanghui Li1
1Department of Oncology, Xinqiao Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Abstract:
Overexpression of ABCG2 is considered a major mechanism of cancer drug resistance. Recent studies have shown that ABCG2 can regulate the switch between symmetric and asymmetric cell division in adult stem cells; however, the relationship between ABCG2 and cell division in drug-resistant cancer cells remains to be determined. In the present study, we demonstrated that ABCG2 is involved in the cell division of drug-resistant cancer cells. We first established drug-resistant H460 and A549 cell lines by repeated exposure to cisplatin and found that the expression of ABCG2 in these cell lines was significantly increased. As evidenced by PKH-26 staining, these drug-resistant cell lines favored symmetric division, which differed from the asymmetric division of the parental cells. Furthermore, we established stable ABCG2‑overexpressing and stable shRNA-ABCG2‑knockdown cell lines to evaluate the potential role of ABCG2 in cancer cell division. The results showed that overexpression of ABCG2 in A549 parental cells significantly increased the proportion of symmetric division, whereas knockdown of ABCG2 in drug-resistant A549 cells significantly increased the proportion of asymmetric division. Taken together, our findings suggest that ABCG2 is involved in the modulation of cancer drug resistance by regulating the pattern of cell division. The present study provides novel insight into the role of ABCG2 in cancer treatment resistance.
Insights
Overexpression of ABCG2 (ATP-binding cassette sub-family G member 2) drives cancer drug resistance by promoting symmetric cell division. Targeting ABCG2 may restore asymmetric division and overcome treatment resistance.
Area of Science:
- Cancer Biology
- Cellular Biology
- Molecular Oncology
Background:
- ATP-binding cassette sub-family G member 2 (ABCG2) is a key factor in cancer drug resistance.
- ABCG2's role in regulating cell division patterns in cancer remains unclear.
- Previous research linked ABCG2 to symmetric/asymmetric division in stem cells.
Purpose of the Study:
- To investigate the role of ABCG2 in cell division patterns of drug-resistant cancer cells.
- To determine if ABCG2 influences the switch between symmetric and asymmetric cell division in acquired drug resistance.
- To elucidate the mechanistic link between ABCG2, cell division, and cancer treatment resistance.
Main Methods:
- Established cisplatin-resistant H460 and A549 cell lines via repeated drug exposure.
- Quantified ABCG2 expression levels in parental and resistant cell lines.
- Utilized PKH-26 staining to assess cell division patterns (symmetric vs. asymmetric).
- Created stable cell lines with either ABCG2 overexpression or ABCG2 knockdown (shRNA).
Main Results:
- Drug-resistant cell lines exhibited significantly increased ABCG2 expression compared to parental cells.
- Resistant cell lines predominantly underwent symmetric cell division, unlike parental cells.
- Overexpression of ABCG2 in parental cells increased symmetric division.
- Knockdown of ABCG2 in resistant cells promoted asymmetric division.
Conclusions:
- ABCG2 plays a significant role in regulating cell division patterns in drug-resistant cancer cells.
- ABCG2 promotes symmetric cell division, contributing to acquired cancer drug resistance.
- Modulating ABCG2 activity could be a therapeutic strategy to overcome cancer treatment resistance by altering cell division.
- This study offers new insights into ABCG2's function in cancer therapy resistance.
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