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Gene Review

ST3  -  suppression of tumorigenicity 3

Homo sapiens

Synonyms: CCTS, TSHL
 
 
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Disease relevance of ST3

  • There was a positive and significant correlation between CCT and ST1 (r=0.27, P=0.001) but not between CCT and ST2 (r=0.02, P=0.8), ST3 (r=0.06, P=0.5), refractive error (r=0.08, P=0.3), or axial length (r=0.07, P=0.4) [1].
  • ST3 expression appeared to be specifically associated with mammary stroma fibroblasts derived from post-radiation fibrosis lesions [2].
  • The complete nucleotide sequence of the fourth gene of symptomatic (Wa, DS-1, P, and VA70) and asymptomatic (M37, 1076, McN13, and ST3) rotaviruses of serotype 1, 2, 3, or 4 was determined by the dideoxy chain termination method [3].
  • We conclude that in esophageal cancer, ST3 might help to assess survival and the risk of recurrence after surgical resection [4].
  • Stromelysin 3 (ST3) is a matrix metalloprotease (MMP) expressed in fibroblast-like cells of most human invasive carcinomas [5].
 

High impact information on ST3

  • Earlier studies suggest that ST3 is a direct T3 response gene, although a thyroid hormone response element (TRE) was not found in the initial analysis of the ST3 promoter [6].
  • The Xenopus laevis ST3 is highly up-regulated by thyroid hormone (T3) during amphibian metamorphosis, and its expression is spatially and temporally correlated with apoptosis in different tissues [6].
  • Here, we have identified a strong TRE consisting of two nearly perfect direct repeats of the consensus nuclear hormone receptor binding element AGGTCA separated by 4 bp in the first intron of the Xenopus ST3 gene [6].
  • These results indicate that hST-3 may regulate IGF-I bioavailability by proteolyzing IGFBP, thus favoring cell survival and proliferation [7].
  • The ST3, BM-40/SPARC, and MET genes were found to be overexpressed in tumor samples compared to control mucosa [4].
 

Chemical compound and disease context of ST3

 

Biological context of ST3

 

Anatomical context of ST3

  • Under similar coculture conditions and using the same cancer cell line stimulation, ST3 expression was, however, quite variable among these 9 cases, reflecting the difference of protease expression observed on the sections of the original tumors [13].
  • The results showed that ST3 expression by stromal cells was cancer-specific [13].
  • Normal breast tissues did not express ST3, and ST3 expression was detected in only 1 of 20 normal axillary lymph nodes [12].
  • ST3 was also expressed in cells cultured from precancerous and cancerous lesions that had undergone epithelial-to-mesenchymal transition [14].
  • ST3 expression in oral hyperplastic and dysplastic lesions suggests its association with progression of phenotypic alterations acquired early during the malignant transformation pathway of oral epithelium and implicates it not only in angiogenesis and invasion but also in tumorigenesis [14].
 

Associations of ST3 with chemical compounds

  • Digoxigenin (DIG)-labelled cDNA probes derived from the VP4 gene of the standard strains RV5 (P4), ST3 (P6) and RV4 (P8) were used to discriminate between the different alleles [15].
  • CD64- monocytes showed lower activity in the phagocytosis of unopsonized particles and also lower zymosan- or latex-induced chemiluminescence than CD64+ monocytes [16].
  • CD64- monocytes pretreated with PPD (purified protein derivative of tuberculin) induced up to tentimes more interferon-gamma and also higher proliferation in responding autologous T cells than PPD-pretreated CD64+ monocytes [16].
 

Other interactions of ST3

  • Of these samples, 70, 62, and 85% showed inhibitory activity against serotype (ST) 1 human RV, ST4 human RV, and ST3 simian RV, respectively; the median titers were 10, 10, and 20, respectively [17].
 

Analytical, diagnostic and therapeutic context of ST3

  • In contrast, ST3 expression, identified by immunohistochemistry in fibroblastic cells surrounding neoplastic islets, correlated with tumor size and periesophageal tissue invasion [4].
  • Of the 36 patients studied, those with high ST3 levels had shorter disease-free survival than those with low levels, but there was no relationship between the cpTNE and disease recurrence or survival [4].
  • Digital image analysis of the dark-field in situ hybridization signal was used to measure the maximal level of ST3 expression in each tumor [8].
  • Confirmation that this ST3 promoter activation results in ST3 gene induction of a similar magnitude was shown using Northern blotting of stimulated fibroblasts [11].
  • However, after direct coculture with cancer cells, expression of ST3 transcripts reappeared in 8 of the 9 cases and was observed only in fibroblasts located in close contact with tumor cells [13].

References

  1. Central corneal thickness is not related to anterior scleral thickness or axial length. Oliveira, C., Tello, C., Liebmann, J., Ritch, R. Journal of glaucoma. (2006) [Pubmed]
  2. Evaluation of quantitative variation in gene expression. Spanakis, E., Brouty-Boyé, D. Nucleic Acids Res. (1994) [Pubmed]
  3. Sequence of the fourth gene of human rotaviruses recovered from asymptomatic or symptomatic infections. Gorziglia, M., Green, K., Nishikawa, K., Taniguchi, K., Jones, R., Kapikian, A.Z., Chanock, R.M. J. Virol. (1988) [Pubmed]
  4. Overexpression of stromelysin-3, BM-40/SPARC, and MET genes in human esophageal carcinoma: implications for prognosis. Porte, H., Triboulet, J.P., Kotelevets, L., Carrat, F., Prévot, S., Nordlinger, B., DiGioia, Y., Wurtz, A., Comoglio, P., Gespach, C., Chastre, E. Clin. Cancer Res. (1998) [Pubmed]
  5. High levels of stromelysin-3 correlate with poor prognosis in patients with breast carcinoma. Chenard, M.P., O'Siorain, L., Shering, S., Rouyer, N., Lutz, Y., Wolf, C., Basset, P., Bellocq, J.P., Duffy, M.J. Int. J. Cancer (1996) [Pubmed]
  6. Transcriptional regulation of the Xenopus laevis Stromelysin-3 gene by thyroid hormone is mediated by a DNA element in the first intron. Fu, L., Tomita, A., Wang, H., Buchholz, D.R., Shi, Y.B. J. Biol. Chem. (2006) [Pubmed]
  7. Identification of insulin-like growth factor-binding protein-1 as a potential physiological substrate for human stromelysin-3. Mañes, S., Mira, E., Barbacid, M.M., Ciprés, A., Fernández-Resa, P., Buesa, J.M., Mérida, I., Aracil, M., Márquez, G., Martínez-A, C. J. Biol. Chem. (1997) [Pubmed]
  8. Correlation between stromelysin-3 mRNA level and outcome of human breast cancer. Engel, G., Heselmeyer, K., Auer, G., Bäckdahl, M., Eriksson, E., Linder, S. Int. J. Cancer (1994) [Pubmed]
  9. Identification of conserved domains in the cell attachment proteins of the three serotypes of reovirus. Duncan, R., Horne, D., Cashdollar, L.W., Joklik, W.K., Lee, P.W. Virology (1990) [Pubmed]
  10. Serum haptoglobin and ferritin during a competitive running and swimming season. Pizza, F.X., Flynn, M.G., Boone, J.B., Rodriguez-Zayas, J.R., Andres, F.F. International journal of sports medicine. (1997) [Pubmed]
  11. Modulation of human stromelysin 3 promoter activity and gene expression by human breast cancer cells. Ahmad, A., Marshall, J.F., Basset, P., Anglard, P., Hart, I.R. Int. J. Cancer (1997) [Pubmed]
  12. Expression of stromelysin-3 and nm23 in breast carcinoma and related tissues. Hähnel, E., Dawkins, H., Robbins, P., Hähnel, R. Int. J. Cancer (1994) [Pubmed]
  13. Stromelysin-3 expression by mammary tumor-associated fibroblasts under in vitro breast cancer cell induction. Wang, C.S., Têtu, B. Int. J. Cancer (2002) [Pubmed]
  14. Stromelysin-3 expression is an early event in human oral tumorigenesis. Soni, S., Mathur, M., Shukla, N.K., Deo, S.V., Ralhan, R. Int. J. Cancer (2003) [Pubmed]
  15. Use of non-radioactive probes for VP4 typing of human rotaviruses. Gorrell, R.J., Palombo, E.A. J. Virol. Methods (1996) [Pubmed]
  16. Phenotypical and functional characterization of Fc gamma receptor I (CD64)-negative monocytes, a minor human monocyte subpopulation with high accessory and antiviral activity. Grage-Griebenow, E., Lorenzen, D., Fetting, R., Flad, H.D., Ernst, M. Eur. J. Immunol. (1993) [Pubmed]
  17. Rotavirus-inhibitory activity in serial milk samples from Mexican women and rotavirus infections in their children during their first year of life. Brüssow, H., Benitez, O., Uribe, F., Sidoti, J., Rosa, K., Cravioto, A. J. Clin. Microbiol. (1993) [Pubmed]
 
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