Role of Bcl‑2 on drug resistance in breast cancer polyploidy‑induced spindle poisons
- Bibo Yuan
- Juan Hao
- Qian Zhang
- Yan Wang
- Yu Zhu
Affiliations: Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Department of Gynecology and Obstetrics, Peking University People's Hospital, Beijing 100044, P.R. China, Department of Gynecology and Obstetrics, Tianjin Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, P.R. China, Department of Gynecology and Obstetrics, Tianjin Jinghai Hospital, Tianjin 301600, P.R. China, Department of Clinical Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, P.R. China
- Published online on: January 7, 2020 https://doi.org/10.3892/ol.2020.11256
Copyright: © Yuan
et al. This is an open access article distributed under the
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Spindle poisons are chemotherapeutic drugs used in the treatment of malignant tumors; however, numerous patients develop resistance following chemotherapy. The present study aimed to induce polyploidy in breast cancer cells using the spindle poison nocodazole to investigate the mechanism of polyploid‑induced tumor resistance. It was revealed that the spindle poison nocodazole induced apoptosis in HCC1806 cells but also induced polyploidy in MDA‑MB‑231 cells. The drug sensitivities of the polyploid MDA‑MB‑231 cells to paclitaxel, docetaxel, epirubicin, 5‑fluorouracil and oxaliplatin were lower than those of the original tumor cells; however, the polyploid MDA‑MB‑231 cells were more sensitive to etoposide than the original tumor cells. The expression of F‑box and WD repeat domain containing 7 (FBW7) was decreased, while the expression of MCL1 apoptosis regulator BCL2 family member (MCL‑1) and Bcl‑2 was increased, and caspase‑3/9 and Bax were not expressed in MDA‑MB‑231 cells. The resistance to docetaxel and etoposide was reversed, but the sensitivity of paclitaxel was not changed following Bcl‑2 silencing. The formation of polyploidy in tumors may be one of the molecular mechanisms underlying tumor resistance to spindle poisons. Expression of the Bcl‑2 family members, for example FBW7 and MCL‑1, plays a key role in apoptosis and the cell escape process that forms polyploid cells. However, Bcl‑2 silencing has different reversal effects on different anti‑tumor drugs, which requires further investigation.