Suppr超能文献

Tsg101对于胚胎组织和成年组织的细胞生长、增殖及细胞存活至关重要。

Tsg101 is essential for cell growth, proliferation, and cell survival of embryonic and adult tissues.

作者信息

Wagner Kay-Uwe, Krempler Andrea, Qi Yongyue, Park KyungRan, Henry MaLinda D, Triplett Aleata A, Riedlinger Gregory, Rucker III Edmund B, Hennighausen Lothar

机构信息

Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha 68198-6805, USA.

出版信息

Mol Cell Biol. 2003 Jan;23(1):150-62. doi: 10.1128/MCB.23.1.150-162.2003.

Abstract

Tumor susceptibility gene 101 (Tsg101) was identified in a random mutagenesis screen for potential tumor suppressors in NIH 3T3 cells. Altered transcripts of this gene have been detected in sporadic breast cancers and many other human malignancies. However, the involvement of this gene in neoplastic transformation and tumorigenesis is still elusive. Using gene targeting, we generated genetically engineered mice with a floxed allele of Tsg101. We investigated essential functions of this gene in vivo and examined whether the loss of function of Tsg101 results in tumorigenesis. Conventional knockout mice were generated through Cre-mediated excision of the first coding exon in the germ line of mouse mammary tumor virus (MMTV)-Cre transgenic mice. The complete ablation of Tsg101 in the developing embryo resulted in death around implantation. In contrast, mammary gland-specific knockout mice developed normally but were unable to nurse their young as a result of impaired mammogenesis during late pregnancy. Neither heterozygous null mutants nor somatic knockout mice developed mammary tumors after a latency of 2 years. The Cre-mediated deletion of Tsg101 in primary cells demonstrated that this gene is essential for the growth, proliferation, and survival of mammary epithelial cells. In summary, our results suggest that Tsg101 is required for normal cell function of embryonic and adult tissues but that this gene is not a tumor suppressor for sporadic forms of breast cancer.

摘要

肿瘤易感基因101(Tsg101)是在对NIH 3T3细胞中潜在肿瘤抑制因子的随机诱变筛选中被鉴定出来的。在散发性乳腺癌和许多其他人类恶性肿瘤中已检测到该基因的转录本改变。然而,该基因在肿瘤转化和肿瘤发生中的作用仍不明确。我们利用基因打靶技术,构建了Tsg101等位基因带有loxP位点的基因工程小鼠。我们研究了该基因在体内的基本功能,并检测Tsg101功能缺失是否会导致肿瘤发生。通过在小鼠乳腺肿瘤病毒(MMTV)-Cre转基因小鼠的种系中经Cre介导切除第一个编码外显子,产生了传统的基因敲除小鼠。发育中的胚胎中Tsg101的完全缺失导致在着床前后死亡。相比之下,乳腺特异性敲除小鼠发育正常,但由于妊娠后期乳腺发育受损而无法哺育幼崽。杂合性无效突变体和体细胞敲除小鼠在2年的潜伏期后均未发生乳腺肿瘤。在原代细胞中经Cre介导删除Tsg101表明,该基因对乳腺上皮细胞的生长、增殖和存活至关重要。总之,我们的结果表明,Tsg101是胚胎和成年组织正常细胞功能所必需的,但该基因不是散发性乳腺癌的肿瘤抑制因子。

相似文献

1
Tsg101 is essential for cell growth, proliferation, and cell survival of embryonic and adult tissues.
Mol Cell Biol. 2003 Jan;23(1):150-62. doi: 10.1128/MCB.23.1.150-162.2003.
3
Targeted deletion of the Tsg101 gene results in cell cycle arrest at G1/S and p53-independent cell death.
J Biol Chem. 2002 Nov 8;277(45):43216-23. doi: 10.1074/jbc.M207662200. Epub 2002 Aug 29.
4
p53 accumulation, defective cell proliferation, and early embryonic lethality in mice lacking tsg101.
Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1859-64. doi: 10.1073/pnas.98.4.1859.
5
Impaired alveologenesis and maintenance of secretory mammary epithelial cells in Jak2 conditional knockout mice.
Mol Cell Biol. 2004 Jun;24(12):5510-20. doi: 10.1128/MCB.24.12.5510-5520.2004.
8
Analysis of expression and structure of the TSG101 gene in cervical cancer cells.
Int J Mol Med. 2010 May;25(5):777-83. doi: 10.3892/ijmm_00000404.
9
Characterization of WWOX inactivation in murine mammary gland development.
J Cell Physiol. 2013 Jul;228(7):1391-6. doi: 10.1002/jcp.24310.

引用本文的文献

1
Overexpression of TSG101 causes the development of adenosquamous mammary carcinoma.
Breast Cancer Res. 2025 Jul 7;27(1):126. doi: 10.1186/s13058-025-02007-8.
2
Neuronal Deletion of () Causes Rapid Apoptotic Loss of Hippocampal CA3 Neurons.
Biomolecules. 2025 May 28;15(6):786. doi: 10.3390/biom15060786.
3
Obese Adipose Tissue Extracellular Vesicles Activate Mitochondrial Fatty Acid β-oxidation to Drive Colonic Stemness.
Cell Mol Gastroenterol Hepatol. 2025;19(7):101504. doi: 10.1016/j.jcmgh.2025.101504. Epub 2025 Mar 22.
4
Schwann cell deletion of ( ) in mice results in severe peripheral neuropathy.
MicroPubl Biol. 2025 Feb 21;2025. doi: 10.17912/micropub.biology.001406. eCollection 2025.
5
Loss of HD-PTP function results in lipodystrophy, defective cellular signaling and altered lipid homeostasis.
J Cell Sci. 2024 Sep 15;137(18). doi: 10.1242/jcs.262032. Epub 2024 Sep 27.
7
Maternal circadian rhythm disruption affects neonatal inflammation via metabolic reprograming of myeloid cells.
Nat Metab. 2024 May;6(5):899-913. doi: 10.1038/s42255-024-01021-y. Epub 2024 Apr 1.
8
Multifaceted effects of milk-exosomes (Mi-Exo) as a modulator of scar-free wound healing.
Nanoscale Adv. 2020 Nov 30;3(2):528-537. doi: 10.1039/d0na00665c. eCollection 2021 Jan 26.
9
Peripubertal requirement of Tsg101 in maintaining the integrity of membranous structures in mouse oocytes.
Cell Prolif. 2022 Oct;55(10):e13288. doi: 10.1111/cpr.13288. Epub 2022 Jun 29.
10
Epstein-Barr Virus Enhances Cancer-Specific Aberrant Splicing of TSG101 Pre-mRNA.
Int J Mol Sci. 2022 Feb 24;23(5):2516. doi: 10.3390/ijms23052516.

本文引用的文献

1
Targeted deletion of the Tsg101 gene results in cell cycle arrest at G1/S and p53-independent cell death.
J Biol Chem. 2002 Nov 8;277(45):43216-23. doi: 10.1074/jbc.M207662200. Epub 2002 Aug 29.
2
Negative regulation of cell growth and differentiation by TSG101 through association with p21(Cip1/WAF1).
Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5430-5. doi: 10.1073/pnas.082123999. Epub 2002 Apr 9.
5
Tsg101 and the vacuolar protein sorting pathway are essential for HIV-1 budding.
Cell. 2001 Oct 5;107(1):55-65. doi: 10.1016/s0092-8674(01)00506-2.
6
7
Tumor susceptibility of p21(Waf1/Cip1)-deficient mice.
Cancer Res. 2001 Aug 15;61(16):6234-8.
8
Growth inhibition and DNA damage induced by Cre recombinase in mammalian cells.
Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9209-14. doi: 10.1073/pnas.161269798.
10
p53 accumulation, defective cell proliferation, and early embryonic lethality in mice lacking tsg101.
Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1859-64. doi: 10.1073/pnas.98.4.1859.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验