DMS 114

DMS 114是人类非小细胞肺癌（英语：Non-small-cell lung carcinoma）细胞系，最初是分离自一名尚未接受治疗的68岁白人男性非小细胞肺癌患者。DMS 114细胞的早期传代曾被莱氏无胆甾原体（英语：Acholeplasma laidlawii）污染，而该莱氏无胆甾原体则在冷冻保存之前已被卡纳霉素等治愈。

科研用途

2008年，有研究指出在治疗中使用β-羟基异戊基紫草苷（一种蛋白酪氨酸激酶的三磷酸腺苷非竞争性抑制剂（英语：Non-competitive inhibition）），可以诱导DMS114细胞凋亡，并且其磷蛋白部分中的dUTPase（英语：dUTP diphosphatase）会减少。同时又发现经5-氟尿嘧啶（一种用作化疗药物的胸苷酸合酶（英语：Thymidylate synthase）的特异性抑制剂）处理的DMS114细胞会被其抑制。这些实验结果表明，dUTPase的活性是导致肺癌细胞死亡的其中一个关键因素^[1]。2011年，有科研人员指出DMS-114细胞最初来自未曾接受过治疗的非小细胞肺癌患者，从而能够确定新化合物的特异性作用^[2]。他们使用发光法 (luminometry) 和生物冷光测定法（英语：Bioluminescence imaging），观察到此细胞系的发光信号 (luminescence signals) 与细胞数量之间的直接关系，并且发现与基于MTT的传统细胞存活率分析相比，生物冷光测定法的灵敏度更高^[3]。2017年，有学者为了研究抗成纤维细胞生长因子 (FGFR) 抑制的潜在机制，以DMS114细胞进行实验，发现其对三种不同的FGFR抑制剂高度敏感，但在治疗中仍表现出持续的残余细胞活性，表明DMS114细胞有着耐药细胞的亚群^[4]。

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参考资料

[1]
Kajimoto, S; Horie, M; Manabe, H; Masuda, Y; Shibayama-Imazu, T; Nakajo, S; Gong, XF; Obama, T; Itabe, H; Nakaya, K. A tyrosine kinase inhibitor, beta-hydroxyisovalerylshikonin, induced apoptosis in human lung cancer DMS114 cells through reduction of dUTP nucleotidohydrolase activity.. Biochimica et biophysica acta. 2008-01, 1782 (1): 41–50 [2019-12-21]. PMID 18078828. doi:10.1016/j.bbadis.2007.11.004. （原始内容存档于2019-12-21）.
[2]
Pettengill, OS; Sorenson, GD; Wurster-Hill, DH; Curphey, TJ; Noll, WW; Cate, CC; Maurer, LH. Isolation and growth characteristics of continuous cell lines from small-cell carcinoma of the lung.. Cancer. 1980-03-01, 45 (5): 906–18 [2019-12-21]. PMID 6266631. doi:10.1002/1097-0142(19800301)45:5<906::aid-cncr2820450513>3.0.co;2-h. （原始内容存档于2019-12-21）.
[3]
Improgo, MR; Johnson, CW; Tapper, AR; Gardner, PD. Bioluminescence-based high-throughput screen identifies pharmacological agents that target neurotransmitter signaling in small cell lung carcinoma.. PloS one. 2011, 6 (9): e24132 [2019-12-21]. PMID 21931655. doi:10.1371/journal.pone.0024132.
[4]
Malchers, F; Ercanoglu, M; Schütte, D; Castiglione, R; Tischler, V; Michels, S; Dahmen, I; Brägelmann, J; Menon, R; Heuckmann, JM; George, J; Ansén, S; Sos, ML; Soltermann, A; Peifer, M; Wolf, J; Büttner, R; Thomas, RK. Mechanisms of Primary Drug Resistance in FGFR1-Amplified Lung Cancer.. Clinical cancer research : an official journal of the American Association for Cancer Research. 2017-09-15, 23 (18): 5527–5536 [2019-12-21]. PMID 28630215. doi:10.1158/1078-0432.CCR-17-0478. （原始内容存档于2019-12-21）.

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外部链接

Cellosaurus entry for DMS 114（页面存档备份，存于互联网档案馆）

[1] [1]
Kajimoto, S; Horie, M; Manabe, H; Masuda, Y; Shibayama-Imazu, T; Nakajo, S; Gong, XF; Obama, T; Itabe, H; Nakaya, K. A tyrosine kinase inhibitor, beta-hydroxyisovalerylshikonin, induced apoptosis in human lung cancer DMS114 cells through reduction of dUTP nucleotidohydrolase activity.. Biochimica et biophysica acta. 2008-01, 1782 (1): 41–50 [2019-12-21]. PMID 18078828. doi:10.1016/j.bbadis.2007.11.004. （原始内容存档于2019-12-21）.

[2] [2]
Pettengill, OS; Sorenson, GD; Wurster-Hill, DH; Curphey, TJ; Noll, WW; Cate, CC; Maurer, LH. Isolation and growth characteristics of continuous cell lines from small-cell carcinoma of the lung.. Cancer. 1980-03-01, 45 (5): 906–18 [2019-12-21]. PMID 6266631. doi:10.1002/1097-0142(19800301)45:5<906::aid-cncr2820450513>3.0.co;2-h. （原始内容存档于2019-12-21）.

[3] [3]
Improgo, MR; Johnson, CW; Tapper, AR; Gardner, PD. Bioluminescence-based high-throughput screen identifies pharmacological agents that target neurotransmitter signaling in small cell lung carcinoma.. PloS one. 2011, 6 (9): e24132 [2019-12-21]. PMID 21931655. doi:10.1371/journal.pone.0024132.

[4] [4]
Malchers, F; Ercanoglu, M; Schütte, D; Castiglione, R; Tischler, V; Michels, S; Dahmen, I; Brägelmann, J; Menon, R; Heuckmann, JM; George, J; Ansén, S; Sos, ML; Soltermann, A; Peifer, M; Wolf, J; Büttner, R; Thomas, RK. Mechanisms of Primary Drug Resistance in FGFR1-Amplified Lung Cancer.. Clinical cancer research : an official journal of the American Association for Cancer Research. 2017-09-15, 23 (18): 5527–5536 [2019-12-21]. PMID 28630215. doi:10.1158/1078-0432.CCR-17-0478. （原始内容存档于2019-12-21）.

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