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乳腺癌中RAB25表达缺失。

Loss of RAB25 expression in breast cancer.

作者信息

Cheng Ji-Ming, Ding Ming, Aribi Ahmed, Shah Prabodh, Rao Krishna

机构信息

Division of Hematology and Oncology, Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, 62794, USA.

出版信息

Int J Cancer. 2006 Jun 15;118(12):2957-64. doi: 10.1002/ijc.21739.

Abstract

A novel breast cancer cell line (RAO-3) was established by transduction of the Q61L mutant RAS into human mammary epithelial cells that were immortalized with catalytic subunit of telomerase (hTERT). The cells displayed anchorage-independent growth and proliferation, and formed human mammary spindle cell carcinoma when injected into nude mice. Chromosome locus 1q22-23 was partially duplicated and inverted on one of the 3 chromosomes present in the cell line. We report here that mutations of chromosome 1q22-23 locus have resulted in the loss of RAB25 expression in the breast cancer cell line. Transduction of RAB25 into the breast cancer cell line arrests anchorage-independent growth. We have also demonstrated loss of RAB25 in human breast tumor tissue. These data suggest that loss of RAB25 might contribute to tumorigenesis of breast cancer, and RAB25 is likely to be an important factor in the development of breast cancer. RAB25 could be used as biological marker of breast cancer and provides a target for gene replacement therapy.

摘要

通过将Q61L突变型RAS转导到用人端粒酶催化亚基(hTERT)永生化的人乳腺上皮细胞中,建立了一种新的乳腺癌细胞系(RAO-3)。这些细胞表现出不依赖贴壁的生长和增殖能力,注射到裸鼠体内时可形成人乳腺梭形细胞癌。在该细胞系的3条染色体中的一条上,染色体位点1q22 - 23发生了部分重复和倒位。我们在此报告,1q22 - 23位点的突变导致该乳腺癌细胞系中RAB25表达缺失。将RAB25转导到该乳腺癌细胞系中可抑制不依赖贴壁的生长。我们还证实了人乳腺肿瘤组织中存在RAB25缺失。这些数据表明,RAB25缺失可能有助于乳腺癌的发生,RAB25可能是乳腺癌发展中的一个重要因素。RAB25可作为乳腺癌的生物标志物,并为基因替代治疗提供靶点。

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