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Gene Review

SEMA3B  -  sema domain, immunoglobulin domain (Ig),...

Homo sapiens

Synonyms: LUCA-1, SEMA5, SEMAA, SemA, Sema A(V), ...
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Disease relevance of SEMA3B


High impact information on SEMA3B

  • Research into the origins of introns is at a critical juncture in the resolution of theories on the evolution of early life (which came first, RNA or DNA?), the identity of LUCA (the last universal common ancestor, was it prokaryotic- or eukaryotic-like?), and the significance of noncoding nucleotide variation [6].
  • We studied the mechanism of SEMA3B-induced tumor cell apoptosis and found that vascular endothelial growth factor (VEGF)165 significantly decreased the proapoptotic and antimitotic effect of transfected or secreted SEMA3B on lung and breast cancer cells [3].
  • VEGF165 binds to neuropilin, receptors for SEMA3B, and we found that SEMA3B competed for binding of 125I-VEGF165 to lung and breast cancer cells [3].
  • The common method of inactivation of SEMA3B is by allele loss and tumor-acquired promoter methylation [3].
  • Semaphorins SEMA3B and its homologue SEMA3F are 3p21.3 candidate tumor suppressor genes (TSGs), the expression of which is frequently lost in lung cancers [7].

Chemical compound and disease context of SEMA3B


Biological context of SEMA3B


Anatomical context of SEMA3B

  • The presence of hypermethylation was statistically associated with loss of SEMA3B expression in both cell lines (P = 0.02) and primary tumors (P < 0.01) [8].

Associations of SEMA3B with chemical compounds


Other interactions of SEMA3B

  • In conclusion, we hypothesize that VEGF165, produced by tumor cells, acts as an autocrine survival factor and that SEMA3B mediates its tumor-suppressing effects, at least in part, by blocking this VEGF autocrine activity [3].
  • Previously, the RASSF1A, BLU and SEMAPHORIN 3B (SEMA3B) candidate tumor suppressor genes on chromosome 3p21.3 were found to be inactivated and downregulated by genetic and epigenetic changes in lung cancer [5].
  • Alterations in 3p tumor suppression genes (TSGs) appear especially early, including those of RASSF1A and SEMA3B at 3p21.3, followed by changes in 9p (p16), 8p, and then multiple other sites [9].
  • In addition, some genes were up-regulated, including matrix metalloproteinse 2(MMP-2), MMP-16(MT3-MMP), SKY, CD9 and semaphorin V [10].

Analytical, diagnostic and therapeutic context of SEMA3B

  • Applying quantitative methylation specific PCR (QMSP) we analyzed bronchial aspirates from 75 patients with primary lung cancer and 64 bronchial aspirates of patients diagnosed with benign lung disease for promoter methylation of 3 candidate marker genes (p16(INK4a), RARB2 and SEMA3B) [11].


  1. Expression of semaphorins, vascular endothelial growth factor, and their common receptor neuropilins and alleic loss of semaphorin locus in epithelial ovarian neoplasms: increased ratio of vascular endothelial growth factor to semaphorin is a poor prognostic factor in ovarian carcinomas. Osada, R., Horiuchi, A., Kikuchi, N., Ohira, S., Ota, M., Katsuyama, Y., Konishi, I. Hum. Pathol. (2006) [Pubmed]
  2. Selective suppression of in vivo tumorigenicity by semaphorin SEMA3F in lung cancer cells. Kusy, S., Nasarre, P., Chan, D., Potiron, V., Meyronet, D., Gemmill, R.M., Constantin, B., Drabkin, H.A., Roche, J. Neoplasia (2005) [Pubmed]
  3. Semaphorin 3B (SEMA3B) induces apoptosis in lung and breast cancer, whereas VEGF165 antagonizes this effect. Castro-Rivera, E., Ran, S., Thorpe, P., Minna, J.D. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  4. Human Semaphorin 3B (SEMA3B) located at chromosome 3p21.3 suppresses tumor formation in an adenocarcinoma cell line. Tse, C., Xiang, R.H., Bracht, T., Naylor, S.L. Cancer Res. (2002) [Pubmed]
  5. Allele loss and epigenetic inactivation of 3p21.3 in malignant liver tumors. Tischoff, I., Markwarth, A., Witzigmann, H., Uhlmann, D., Hauss, J., Mirmohammadsadegh, A., Wittekind, C., Hengge, U.R., Tannapfel, A. Int. J. Cancer (2005) [Pubmed]
  6. Origins and evolution of spliceosomal introns. Rodr??guez-Trelles, F., Tarr??o, R., Ayala, F.J. Annu. Rev. Genet. (2006) [Pubmed]
  7. Inhibition of lung cancer cell growth and induction of apoptosis after reexpression of 3p21.3 candidate tumor suppressor gene SEMA3B. Tomizawa, Y., Sekido, Y., Kondo, M., Gao, B., Yokota, J., Roche, J., Drabkin, H., Lerman, M.I., Gazdar, A.F., Minna, J.D. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  8. Allelic loss on chromosome 3p21.3 and promoter hypermethylation of semaphorin 3B in non-small cell lung cancer. Kuroki, T., Trapasso, F., Yendamuri, S., Matsuyama, A., Alder, H., Williams, N.N., Kaiser, L.R., Croce, C.M. Cancer Res. (2003) [Pubmed]
  9. Molecular pathogenesis of lung cancer and potential translational applications. Minna, J.D., Fong, K., Zöchbauer-Müller, S., Gazdar, A.F. Cancer journal (Sudbury, Mass.) (2002) [Pubmed]
  10. Profiling of differentially expressed genes in human gastric carcinoma by cDNA expression array. Liu, L.X., Liu, Z.H., Jiang, H.C., Qu, X., Zhang, W.H., Wu, L.F., Zhu, A.L., Wang, X.Q., Wu, M. World J. Gastroenterol. (2002) [Pubmed]
  11. Aberrant promoter methylation of p16(INK4a), RARB2 and SEMA3B in bronchial aspirates from patients with suspected lung cancer. Grote, H.J., Schmiemann, V., Geddert, H., Rohr, U.P., Kappes, R., Gabbert, H.E., Böcking, A. Int. J. Cancer (2005) [Pubmed]
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