Perturbation of TSG101 protein affects cell cycle progression

Qing Zhong, Yumay Chen, Diane Jones, Wen Hwa Lee

Research output: Contribution to journalArticlepeer-review

47 Scopus citations


tsg101 was recently identified as a tumor susceptibility gene by functional inactivation of allelic loci in mouse 3T3 fibroblasts. Although previous studies suggested that homozygous intragenic deletion of TSG101 is rare in breast cancer cells and specimens, the neoplastic phenotype caused by tsg101 inactivation implicated that tsg101 may play a significant role in cell growth control Here, we characterize mouse polyclonal and monoclonal antibodies that specifically recognize the TSG101 protein (molecular mass, 46 kDa) in whole-cell lysates by straight Western blot analysis. By indirect immunofluorescence staining, TSG101 was found to be localized in the cytoplasm throughout the entire cell cycle. However, the nuclear staining increases from G1 to S phase and becomes dominant in late S phase. TSG101 is mainly distributed surrounding the chromosomes during M phase. The expression level of TSG101 is not cell cycle dependent. It is possible that the relocalization of TSG101 from the cytoplasm into the nucleus may be relevant to its function. Microinjection of both polyclonal and monoclonal antibodies specific to TSG101 into cells during G1 or S phase results in cell cycle arrest. Furthermore, overexpression of TSG101 leads to cell death, suggesting that the appropriate amount of TSG101 is critical for cell cycle progression. Taken together, these results suggest that neoplastic transformation caused by TSG101 deficiency may result from bypassing of the cell cycle checkpoints.

Original languageEnglish (US)
Pages (from-to)2699-2702
Number of pages4
JournalCancer Research
Issue number13
StatePublished - Jul 1 1998

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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