Downregulation of missing in metastasis gene (MIM) is associated with the progression of bladder transitional carcinomas

Ying Wang, Jiali Liu, Elizabeth Smith, Kang Zhou, Jie Liao, Guang Yu Yang, Ming Tan, Xi Zhan

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


Missing in metastasis (MIM) gene encodes a putative metastasis suppressor. However, the role of MIM in tumorigenesis and metastasis has not yet been established. Western blot analysis using a MIM specific antibody demonstrated that MIM protein is present at varying levels in a variety of normal cells as well as tumor cell lines. Immunohistochemical staining of adult mouse tissues revealed abundant MIM immunoreactivity in uroepithelial cells in the bladder, neuron Purkinje cells in the cerebellum, and megakaryocytes in the bone marrow and spleen in addition. MIM immunoreactivity also was found in human normal bladder transitional epithelial cells. However, the reactivity was not seen in 69 percent of human primary transitional cell carcinoma specimens. Over 51 percent of the tumors at low grade display MIM staining similarly to the normal cells, whereas only 16.7 percent of the tumors at high-grade with poor differentiation show faint or mild staining. Furthermore, full-length MIM protein is highly expressed in SV-HUC-L an immortalized normal transitional epithelial cell line, moderately expressed in T24 and poorly expressed in J82 and TCCSUP transitional cell carcinoma cells. This finding indicates that downegulation of MIM expression may correlate with the transition of tumor cells from distinct epithelium-like morphology to less differentiated carcinomas.

Original languageEnglish (US)
Pages (from-to)79-86
Number of pages8
JournalCancer Investigation
Issue number2
StatePublished - Mar 2007
Externally publishedYes


  • Bladder transitional carcinomas
  • Gene expression
  • MIM
  • Metastasis

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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