Jiaheng Li,Mei Jiang,Xiaoting Zhao,Ziyu Wang,Meng Gu,Weiying Li. Cisplatin selects for CD133+ cells in lung cancer cells. Oncol Transl Med, 2020, 6: 16-20. |
Cisplatin selects for CD133+ cells in lung cancer cells |
Received:May 06, 2019 Revised:June 10, 2019 |
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KeyWord:CD133;Cisplatin;Lung cancer cells |
Author Name | Affiliation | E-mail | Jiaheng Li | Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | ljhhbmu@126.com | Mei Jiang | Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | | Xiaoting Zhao | Department of Cellular Molecular Biology,Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | | Ziyu Wang | Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | | Meng Gu | Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | | Weiying Li | Beijing Chest Hospital,Capital Medical University,Beijing Tuberculosis and Thoracic Tumor Research Institute | li_weiying412@aliyun.com |
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Abstract: |
Objective Platinum-based chemotherapy is the first-line treatment for non–small cell lung cancer, but the
chemoresistance of tumor cells continues to be a considerable challenge in the management of NSCLCs,
leading to recurrence of most patients. CD133 (prominin-1) is a five-transmembrane glycoprotein, and
recent evidence suggests that CD133+ cells are the cause of drug resistance and tumor recurrence. In this
study, the correlation between cisplatin and CD133+ cells was investigated systematically.
Methods Four lung cancer cell lines, including A549, H460, 801D and H1299, were treated with different
concentrations of cisplatin. Cell viability was determined by MTT assay. Sphere-forming assay was
performed to detect the capability of sphere-forming. CD133+ cells was detected by BD FACScaliber flow
cytometer.
Results The results showed that cisplatin could increase the number of CD133+ cells in both time- and
dose-dependent manner. The enrichment would weaken but the proportion of CD133+ cells was still higher
than the basic level as incubation time extended after cisplatin was withdrawn. Compared with adherent
culture, the proportion of CD133+ cells was higher when the cells were maintained suspension culture.
The proportion of CD133+ cells significantly increased when cisplatin was provided in suspension culture.
Conclusion These results revealed that cisplatin induces the enrichment of CD133+ cells and CD133
is a new therapeutic target. Our data partially explained drug resistance to second-line chemotherapy in
cisplatin-treated patients with NSCLCs. |
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