Anti-Apoptopic Gene SCC-S2 and Diagnostic and Therapeutic Uses Thereof

Section: For Industry

Category(ies): Cancer Therapeutics

Reference #: KAUS430503

OTC Contact: David Humphrey, Ph.D. (Directory Information | Send a Message)

Description

SCC-S2 is a ~21 kDa cytosolic protein expressed in human breast cancer and renal carcinoma cells. SCC-S2 expression was found to be higher (approximately 2-32 fold) in several breast cancer tissue samples as compared to normal adjacent tissues examined from patients. SCC-S2 expression was also higher (approximately 2-68 fold) in most of the renal cell carcinoma samples as compared to normal adjacent tissues examined from patients. While the mechanism of action is unclear, activation of NF-kB leads to enhanced expression of SCC-S2. Systemic treatment of mice with cationic liposomal formulation of SCC-S2 antisense oligo led to decreased incidence of pulmonary metastasis and inhibition of SCC-S2 experiment in vivo. Antisense inhibition of endogenous SCC-S2 3expression correlated with decreased VEGF receptor-2 in tumor cells and human lung microvascular endothelial cells and loss of endothelial cell viability. In addition, downregulation of SCC-S2 expression in tumor cells was associated decreased expression of know metastasis-related molecules MMP-1 and MMP-9.

Applications

Since SCC-S2 plays a role in cell growth regulation in vitro and in vivo, SCC-S2 may be an effective biomarker and prognostic indicator for these cancers and ultimately may be a valuable therapeutic target. 

Advantages

Stage of Development

Inventors: Usha Kasid, Deepak Kumar, Prafulla Gokhale, and Imran Ahmad

Relevant Publications

  • Kumar et al. “Identification of a Novel Tumor Necrosis Factor-a-inducible Gene, SCC-S2, Containing the Consensus Sequence of a Death Effector Domain of Fas-associated Death Domain-like Interleukin-1b-converting Enzyme-inhibitory Protein.”  Journal of Biological Chemistry 275(4): 2973–2978, 2000.
  • Zhang et al.  “Role of SCC-S2 in Experimental Metastasis and Modulation of VEGFR-2, MMP-1, and MMP-9 Expression.” Molecular Therapy 13(5): 947-955, 2006.

Patent Status

U.S. Patent Publication 20070087992