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Updated: Feb 7, 2026

Flow Cytometric Detection of Newly-formed Breast Cancer Stem Cell-like Cells After Apoptosis Reversal
Published on: January 26, 2019
CD155 downregulation synergizes with adriamycin to induce breast cancer cell apoptosis
Jian Gao1,2, Qianqian Zheng1, Yue Shao1
1Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, China.
Abstract:
CD155 has been implicated in migration, invasion, proliferation and apoptosis of human cancer cells, and DNA damage response caused by chemotherapeutic agents or reactive oxygen species has been shown to attribute to CD155 induction. Adriamycin (Adr) is one of the most common chemotherapeutic drugs used to treat breast cancer. Here we reported that treatment with Adr upregulated CD155 expression on several in vitro cultured breast cancer cells and in breast cancer cell 4T1 xenografts. We also found that CD155 knockdown or Adr treatment induced apoptosis of in vitro cultured cancer cells and cancer cells in 4T1 xenografts, and a combination of CD155 knockdown with Adr treatment induced more cell death than either of them. Furthermore, we revealed that the combination of CD155 knockdown with Adr treatment suppressed the growth of 4T1 xenografts more significantly than them alone. In summary, our results demonstrate that CD155 downregulation synergizes with Adr to induce breast cancer cell apoptosis, thereby to suppress tumor growth. Our results also suggest that CD155 upregulation may be a mechanism underlying Adr resistance by breast cancer cells.
Insights
Downregulating CD155 enhances Adriamycin chemotherapy effectiveness against breast cancer. Combining CD155 knockdown with Adriamycin boosts cancer cell death and suppresses tumor growth, suggesting a new therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- CD155 plays a role in cancer cell migration, invasion, proliferation, and apoptosis.
- CD155 expression is induced by DNA damage from chemotherapy or reactive oxygen species.
- Adriamycin (Adr) is a common chemotherapeutic agent for breast cancer.
Purpose of the Study:
- To investigate the effect of Adriamycin on CD155 expression in breast cancer cells.
- To evaluate the combined effect of CD155 knockdown and Adriamycin on breast cancer cell apoptosis and tumor growth.
- To explore CD155's role in Adriamycin resistance.
Main Methods:
- Treatment of in vitro cultured breast cancer cells and 4T1 xenografts with Adriamycin.
- CD155 knockdown using specific techniques.
- Assessment of apoptosis induction and tumor growth suppression.
- Analysis of CD155 expression levels.
Main Results:
- Adriamycin treatment upregulated CD155 expression in breast cancer cells and xenografts.
- Both CD155 knockdown and Adriamycin induced apoptosis; their combination resulted in greater cell death.
- Combined CD155 knockdown and Adriamycin significantly suppressed tumor growth compared to monotherapy.
- CD155 upregulation may contribute to Adriamycin resistance in breast cancer cells.
Conclusions:
- CD155 downregulation synergizes with Adriamycin to enhance breast cancer cell apoptosis and inhibit tumor growth.
- Targeting CD155 in combination with Adriamycin presents a promising therapeutic strategy for breast cancer.
- CD155 upregulation could be a mechanism of resistance to Adriamycin in breast cancer.
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