ESTABLISHMENT AND CHARACTERIZATION OF CELL LINE OF UNDIFFERENTIATED PLEOMORPHIC SARCOMA

Background: Undifferentiated pleomorphic sarcoma (UPS) is an aggressive mesenchymal malignancy. Although patient-derived cell lines are invaluable tools for preclinical studies, there are only a few UPS cell lines available in public cell banks. In the present study, we established a cell line from...

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Published inSoshiki baiyō kenkyū Vol. 36; no. 5; pp. 41 - 48
Main Authors TAKAI, Yoko, OYAMA, Rieko, KITO, Fusako, SAKUMOTO, Marimu, SHIOZAWA, Kumiko, QIAO, Zhiwei, NAKAJIMA, Kosei, TAKAHASHI, Mami, YOSHIDA, Akihiko, SETSU, Nokitaka, KOBAYASHI, Eisuke, KAWAI, Akira, KONDO, Tadashi
Format Journal Article
LanguageEnglish
Published Kyoto The Japanese Tissue Culture Association 01.01.2017
Japan Science and Technology Agency
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Summary:Background: Undifferentiated pleomorphic sarcoma (UPS) is an aggressive mesenchymal malignancy. Although patient-derived cell lines are invaluable tools for preclinical studies, there are only a few UPS cell lines available in public cell banks. In the present study, we established a cell line from the primary tumor tissue of a UPS patient. Methods: Primary UPS tumor tissues were sampled to establish cell lines. Morphological and proteomic analyses were performed and sensitivity to anti-cancer drugs was evaluated. Results: We established a novel UPS cell line, namely NCC-UPS1-C1 cells, and maintained the cells for over 100 passages. The characters of cells as morphology, growth rate, colony formation capacity, and immune-histochemical traits were confirmed. Mass spectrometric protein expression profiling revealed that the proteome of the original tumor tissue differed from that of the cell line. Sensitivity to 164 anti-cancer drugs was screened for their growth inhibitory effects. Conclusions: Patient-derived cell line in this study may be useful for understanding the molecular background of drug resistance in UPS. Furthermore, the use of the patient-derived cancer model will facilitate our understanding of molecular mechanisms underlying poor prognosis, and will contribute to novel therapeutic strategies.
ISSN:0912-3636
1881-3704
DOI:10.11418/jtca.36.41