Differential expression analysis of MIM (MTSS1) splice variants and a functional role of MIM in prostate cancer cell biology

  • Authors:
    • Robert D. Loberg
    • Chris K. Neeley
    • Lashon L. Adam-Day
    • Yaron Fridman
    • Lauren N. St. John
    • Sheri Nixdorf
    • Paul Jackson
    • Linda M. Kalikin
    • Kenneth J. Pienta
  • View Affiliations

  • Published online on: June 1, 2005     https://doi.org/10.3892/ijo.26.6.1699
  • Pages: 1699-1705
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

We previously identified MIM-A (missing in metastasis, MTSS1) by differential display techniques as missing in invasive, metastatic bladder cancer cell lines and suggested that MIM-A is a novel putative metastasis suppressor gene. Characterization of the MIM gene revealed a WH2 (Wiskott-Aldrich syndrome protein homology 2) domain in the C-terminus that is known to bind actin monomers and regulate organization of the actin cytoskeleton. Here, we further describe two alternatively splice variants of MIM-A, called MIM(12del) and MIM-B, which share >50% amino acid sequence homology with MIM-A in the C-terminal domain. We show that expression of all three transcripts is down-regulated in prostate cancer cell lines and tumor samples from patients. In addition, we generated stably-transfected PC-3 cells overexpressing MIM-A to evaluate the importance of MIM-A in prostate cancer biology. The initial experiments show that expression of MIM decreased the number of actin filaments and was associated with a decrease in the G:F actin ratio. Overexpression of MIM-A had no effect on PC-3 cell adhesion to extracellular matrices, as well as no effect on PC-3 motility. Further, overexpression of MIM-A reduced the rate of PC-3 cell proliferation. These results support the hypothesis that MIM-A is an actin-binding protein and implicate a role of MIM-A in the regulation of cellular proliferation. These data suggest that the reduction of MIM-A gene expression in prostate cancer and other cancers may contribute to tumor growth and development, as well as metastasis.

Related Articles

Journal Cover

June 2005
Volume 26 Issue 6

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Loberg RD, Neeley CK, Adam-Day LL, Fridman Y, St. John LN, Nixdorf S, Jackson P, Kalikin LM and Pienta KJ: Differential expression analysis of MIM (MTSS1) splice variants and a functional role of MIM in prostate cancer cell biology. Int J Oncol 26: 1699-1705, 2005
APA
Loberg, R.D., Neeley, C.K., Adam-Day, L.L., Fridman, Y., St. John, L.N., Nixdorf, S. ... Pienta, K.J. (2005). Differential expression analysis of MIM (MTSS1) splice variants and a functional role of MIM in prostate cancer cell biology. International Journal of Oncology, 26, 1699-1705. https://doi.org/10.3892/ijo.26.6.1699
MLA
Loberg, R. D., Neeley, C. K., Adam-Day, L. L., Fridman, Y., St. John, L. N., Nixdorf, S., Jackson, P., Kalikin, L. M., Pienta, K. J."Differential expression analysis of MIM (MTSS1) splice variants and a functional role of MIM in prostate cancer cell biology". International Journal of Oncology 26.6 (2005): 1699-1705.
Chicago
Loberg, R. D., Neeley, C. K., Adam-Day, L. L., Fridman, Y., St. John, L. N., Nixdorf, S., Jackson, P., Kalikin, L. M., Pienta, K. J."Differential expression analysis of MIM (MTSS1) splice variants and a functional role of MIM in prostate cancer cell biology". International Journal of Oncology 26, no. 6 (2005): 1699-1705. https://doi.org/10.3892/ijo.26.6.1699