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T25
KYSE-150/KYSE-150细胞系/KYSE-150细胞株/KYSE-150人食管鳞癌细胞
Cell line name KYSE-150
Synonyms KYSE 150; KYSE150; Kyse150; KY150
Accession CVCL_1348
Resource Identification Initiative To cite this cell line use: KYSE-150 (RRID:CVCL_1348)
Comments Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Population: Japanese.
Doubling time: 13.7 hours (PubMed=1728357); 23 hours (PubMed=25984343); <25 hours (Note=Less when serum amount is increased) (DSMZ=ACC-375).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: CRISPR phenotypic screen.
Omics: Deep exome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: shRNA library screening.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Derived from site: In situ; Esophagus; UBERON=UBERON_0001043.
PubMed=15172977; DOI=10.1158/0008-5472.CAN-04-0172
Sonoda I., Imoto I., Inoue J., Shibata T., Shimada Y., Chin K., Imamura M., Amagasa T., Gray J.W., Hirohashi S., Inazawa J.
Frequent silencing of low density lipoprotein receptor-related protein 1B (LRP1B) expression by genetic and epigenetic mechanisms in esophageal squamous cell carcinoma.
Cancer Res. 64:3741-3747(2004)
PubMed=16045545; DOI=10.1111/j.0959-9673.2005.00431.x; PMCID=PMC2517430
Ban S., Michikawa Y., Ishikawa K.-i., Sagara M., Watanabe K., Shimada Y., Inazawa J., Imai T.
Radiation sensitivities of 31 human oesophageal squamous cell carcinoma cell lines.
Int. J. Exp. Pathol. 86:231-240(2005)
PubMed=16832412; DOI=10.1038/sj.bjc.6603255; PMCID=PMC2360647
Tsunoda S., Okumura T., Ito T., Mori Y., Soma T., Watanabe G., Kaganoi J.-i., Itami A., Sakai Y., Shimada Y.
Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma.
Br. J. Cancer 95:322-330(2006)
PubMed=20164919; DOI=10.1038/nature08768; PMCID=PMC3145113
Bignell G.R., Greenman C.D., Davies H.R., Butler A.P., Edkins S., Andrews J.M., Buck G., Chen L., Beare D., Latimer C., Widaa S., Hinton J., Fahey C., Fu B.-Y., Swamy S., Dalgliesh G.L., Teh B.T., Deloukas P., Yang F.-T., Campbell P.J., Futreal P.A., Stratton M.R.
Signatures of mutation and selection in the cancer genome.
Nature 463:893-898(2010)
PubMed=20215515; DOI=10.1158/0008-5472.CAN-09-3458; PMCID=PMC2881662
Rothenberg S.M., Mohapatra G., Rivera M.N., Winokur D., Greninger P., Nitta M., Sadow P.M., Sooriyakumar G., Brannigan B.W., Ulman M.J., Perera R.M., Wang R., Tam A., Ma X.-J., Erlander M., Sgroi D.C., Rocco J.W., Lingen M.W., Cohen E.E.W., Louis D.N., Settleman J., Haber D.A.
A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers.
Cancer Res. 70:2158-2164(2010)
PubMed=21191746; DOI=10.1007/s11684-010-0260-x
Ji J.-F., Wu K., Wu M., Zhan Q.-M.
p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell lines.
Front. Med. China 4:412-418(2010)
PubMed=22460905; DOI=10.1038/nature11003; PMCID=PMC3320027
Barretina J.G., Caponigro G., Stransky N., Venkatesan K., Margolin A.A., Kim S., Wilson C.J., Lehar J., Kryukov G.V., Sonkin D., Reddy A., Liu M., Murray L., Berger M.F., Monahan J.E., Morais P., Meltzer J., Korejwa A., Jane-Valbuena J., Mapa F.A., Thibault J., Bric-Furlong E., Raman P., Shipway A., Engels I.H., Cheng J., Yu G.-Y.K., Yu J.-J., Aspesi P. Jr., de Silva M., Jagtap K., Jones M.D., Wang L., Hatton C., Palescandolo E., Gupta S., Mahan S., Sougnez C., Onofrio R.C., Liefeld T., MacConaill L.E., Winckler W., Reich M., Li N.-X., Mesirov J.P., Gabriel S.B., Getz G., Ardlie K., Chan V., Myer V.E., Weber B.L., Porter J., Warmuth M., Finan P., Harris J.L., Meyerson M.L., Golub T.R., Morrissey M.P., Sellers W.R., Schlegel R., Garraway L.A.
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
Nature 483:603-607(2012)
PubMed=25984343; DOI=10.1038/sdata.2014.35; PMCID=PMC4432652
Cowley G.S., Weir B.A., Vazquez F., Tamayo P., Scott J.A., Rusin S., East-Seletsky A., Ali L.D., Gerath W.F.J., Pantel S.E., Lizotte P.H., Jiang G.-Z., Hsiao J., Tsherniak A., Dwinell E., Aoyama S., Okamoto M., Harrington W., Gelfand E.T., Green T.M., Tomko M.J., Gopal S., Wong T.C., Li H.-B., Howell S., Stransky N., Liefeld T., Jang D., Bistline J., Meyers B.H., Armstrong S.A., Anderson K.C., Stegmaier K., Reich M., Pellman D., Boehm J.S., Mesirov J.P., Golub T.R., Root D.E., Hahn W.C.
Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies.
Sci. Data 1:140035-140035(2014)
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文献和实验*发表【中文论文】请标注：由博辉生物科技（广州）有限公司提供； *发表【英文论文】请标注：From Bohui Biological Technology (Guangzhou) Co., Ltd.
Nat Methods：殷昊团队开发不依赖 DNA 供体高效靶向插入基因组的新方法：GRAND editing
者们在不同细胞系的多个基因组位点证明，当插入片段大小为 150 bp，精准插入效率可达约 60%，当片段为 250 bp 时，插入效率也高达约 30%，并且此方法所产生的副产物很低，并检测不到脱靶。值得指出的是，研究者们在非分裂细胞中证实 GRAND editing 可以不依赖于 DNA 供体进行长片段序列的精准插入。 研究者们巧妙地利用一对特殊设计的 pegRNAs 来实现目的片段的靶向插入。这两条 pegRNAs 的 3' 端携带的逆转录模板（reverse transcription
PNAS：RAS 抑制剂又添一员，新型蛋白模拟物或为癌症治疗
12X 突变体 H-Ras 与 CHDSos-5 的肽滴定实验表明，蛋白模拟物在类似的低微摩尔亲和力范围内结合所有 Ras 蛋白。随后研究团队评估了 Sos 蛋白模拟物抑制细胞中 Ras 信号转导的潜力。MTT 细胞活性实验发现，与野生型细胞系相比，CHDSos-5 对含有致癌 Ras 突变的细胞系表现出浓度依赖性毒性，并且细胞活性与不同细胞系间固有的巨胞饮摄取水平呈负相关。这些结果表明，利用上调的巨胞饮作用为突变癌细胞提供治疗提供了潜在优势。图片来源：PNAS化学蛋白质组学分析揭示了 CHDSos-5
polybrene。 4、继续培养24小时，用新鲜培养基替换含有病毒的培养基。 5、继续培养。如果慢病毒含有荧光蛋白，一般转染48小时后可见明显荧光表达，72小时后更加明显。如需FACS检测转染效率，可在转染后72-96小时进行。如果慢病毒含有抗性基因并且需要加药筛选，可以在转染3-4天后开始加药。 二、慢病毒转染悬浮细胞实验方法 1、在2×10^5/ml悬浮细胞中加入polybrene至6 μg/ml和适量病毒，充分混匀。37℃孵育。或者150g室温离心4小时
技术资料
