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通过微细胞转移导入人类11号染色体可控制HeLa细胞的致瘤性表达。

Introduction of human chromosome 11 via microcell transfer controls tumorigenic expression of HeLa cells.

作者信息

Saxon P J, Srivatsan E S, Stanbridge E J

出版信息

EMBO J. 1986 Dec 20;5(13):3461-6. doi: 10.1002/j.1460-2075.1986.tb04670.x.

Abstract

Both tumorigenic segregant HeLa X human fibroblast hybrids and tumorigenic HeLa (D98/AH-2) cells can be converted to a non-tumorigenic state following introduction of a single copy of a fibroblast t(X;11) chromosome. The translocated chromosome contains approximately 95% of the 11 chromosome and the q26-qter portion of the X chromosome which contains the hypoxanthine guanine phosphoribosyl transferase (HPRT) gene. Introduction of a human X chromosome has no effect on tumorigenic expression. Suppression of tumorigenicity is relieved by selecting cells which have lost the t(X;11) chromosome by growth in medium containing 6-thioguanine (6-TG). Further, reintroduction of the t(X;11) chromosome into tumorigenic 6TGR cells again suppresses tumorigenicity. Thus, the introduction of a single copy of a human chromosome 11 is sufficient to completely suppress the tumorigenic phenotype of HeLa cells and is suggestive of the presence of tumor-suppressor gene(s) on this chromosome.

摘要

致瘤性分离的HeLa细胞与人类成纤维细胞杂交体以及致瘤性HeLa(D98/AH-2)细胞在导入成纤维细胞t(X;11)染色体的单拷贝后,均可转变为非致瘤状态。易位染色体包含11号染色体约95%的部分以及X染色体的q26-qter部分,该部分包含次黄嘌呤鸟嘌呤磷酸核糖基转移酶(HPRT)基因。导入人类X染色体对致瘤性表达无影响。通过在含有6-硫鸟嘌呤(6-TG)的培养基中培养,筛选出丢失了t(X;11)染色体的细胞,可解除对致瘤性的抑制。此外,将t(X;11)染色体重新导入致瘤性6TGR细胞中,又会再次抑制致瘤性。因此,导入人类11号染色体的单拷贝足以完全抑制HeLa细胞的致瘤表型,这表明该染色体上存在肿瘤抑制基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/545d/1167381/16c4ab733afb/emboj00176-0067-a.jpg

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