TRANSFER OF A NORMAL HUMAN CHROMOSOME-11 SUPPRESSES TUMORIGENICITY OF SOME BUT NOT ALL TUMOR-CELL LINES
TRANSFER OF A NORMAL HUMAN CHROMOSOME-11 SUPPRESSES TUMORIGENICITY OF SOME BUT NOT ALL TUMOR-CELL LINES
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DOI：
10.1002/jcb.240420304
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发表时间：
1990-03-01
影响因子：
4
通讯作者：
BARRETT, JC
中科院分区：
文献类型：
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作者：
OSHIMURA, M;KUGOH, H;BARRETT, JC
Stanbridge及其同事已经证实，通过微细胞融合单染色体t（X;11）引入人宫颈癌细胞（HeLa）和Wilm肿瘤细胞系（G401）后，完全抑制了其致瘤性。为了确定其他肿瘤细胞系是否受到11号染色体的抑制，我们进行了染色体转移实验，通过微细胞融合到各种人类肿瘤细胞系中，包括宫颈癌（SiHa）、横纹肌肉瘤（A204）、子宫内膜癌（HHUA）、肾细胞癌（YCR-1）和大鼠enu诱导的肾母细胞瘤（ENU-T1）。我们首先分离了一个小鼠A9细胞，其中包含一条人类11号染色体，并整合了pSV2-neo质粒DNA。将新标记的11号染色体与上述各种肿瘤进行微细胞融合后，我们分离出抗G418的克隆，并进行核型分析和染色体原位杂交以确保标记染色体的转移。各细胞系亲本细胞均具有高度致瘤性，而SiHa和A204微细胞杂交克隆在裸鼠传代早期无致瘤性，HHUA为中度致瘤性。另一方面，引入11号染色体后，YCR-1和ENU-T1微细胞杂交克隆仍具有较高的致瘤性。因此，引入正常的11号染色体可以抑制部分肿瘤的致瘤性，但并非所有肿瘤的致瘤性，这表明11号染色体上假定的抑制基因的功能仅对特定肿瘤有效。
The complete suppression of tumorigenicity of a human cervical cancer cell (HeLa) and a Wilm''s tumor cell line (G401) following the introduction via microcell fusion of a single chromosome t(X;11) has been demonstrated by Stanbridge and coworkers. To determine whether other tumor cell lines are suppressed by chromosome 11, we performed chromosome transfer experiments via microcell fusion into various human tumor cell lines, including a uterine cervical cacinoma (SiHa), a rhabdomy-osarcoma (A204), a uterine endometrial carcinoma (HHUA), a renal cell carcinoma (YCR-1), and a rat ENU-induced nephroblastoma (ENU-T1). We first isolated a mouse A9 cell containing a single human chromosome 11 with integrated pSV2-neo plasmid DNA. Following microcell fusion of the neo-marked chromosome 11 with the various tumors mentioned above, we isolated clones that were resistant to G418 and performed karyotypic analyses and chromosomal in situ hybridization to ensure the transfer of the marked chromosome. Whereas the parental cells of each cell line were highly tumorigenic, SiHa and A204 microcell hybrid clones at early passages were nontumorigenic in nude mice and HHUA was moderately tumorigenic. On the other hand, YCR-1 and ENU-T1 microcell hybrid clones were still highly tumorigenic following the introduction of chromosome 11. Thus, the introduction of a normal chromosome 11 suppresses the tumorigenic of some but not all tumors, suggesting that the function of the putative suppressor gene(s) on chromosome 11 is effective only in specific tumors.