We demonstrate the potential function of the TSG101∆154-1054 protein in the malignancy of human NPC with scratch-wound healing and transwell invasion assays.
Instead of cancer initiation, it is therefore likely that Tsg101 plays a more predominant role in the progression of a subset of spontaneously arising breast cancers.
Abnormal TSG101 transcripts with highly-specific deletions in the protein-coding region have been identified in human tumor samples and cancer cell lines, including prostate and breast carcinomas, and have been attributed to alternative splicing of TSG101 mRNA.
We found no consistent evidence of aberrant splicing or point mutations in breast cancer or Wilms' tumor suggesting that TSG101 is not a primary target of inactivation in human cancer.
While we cannot exclude that alterations in TSG101 and FHIT occur during cancer development, our data indicate that in this context the commonly observed transcript abnormalities are misleading.