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Gene Review

DLEC1  -  deleted in lung and esophageal cancer 1

Homo sapiens

Synonyms: CFAP81, DLC-1, DLC1, Deleted in lung and esophageal cancer protein 1, Deleted in lung cancer protein 1, ...
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Disease relevance of DLEC1


High impact information on DLEC1

  • These results provide a novel mechanism whereby the SH2 domain of cten-mediated focal adhesion localization of DLC-1 plays an essential role in its tumor suppression activity [4].
  • The phosphotyrosine-independent interaction of DLC-1 and the SH2 domain of cten regulates focal adhesion localization and growth suppression activity of DLC-1 [4].
  • Unexpectedly, the interaction between DLC-1 and the cten SH2 domain is independent of tyrosine phosphorylation of DLC-1 [4].
  • Overlapping double (dlec1) or triple (dlec2) polyadenylation addition signals are found and there is an unusually high degree of homology (84%) between their 3'-untranslated regions.(ABSTRACT TRUNCATED AT 250 WORDS)[5]
  • On the basis of the deduced amino acid sequences and compositions and the mol. wts. of their encoded glycoproteins, the genes, dlec1 and dlec2, are predicted to encode erythro- and leucoagglutinating phytohemagglutinins (PHA-E and PHA-L), respectively [5].

Biological context of DLEC1


Anatomical context of DLEC1


Associations of DLEC1 with chemical compounds

  • Disruption of the complementary interactions in this motif by mutation of F56 to serine, arginine, or glutamate is known to have deleterious effects on catalytic efficiency but remarkably different effects on the stability of the dimer [Hornby et al. (2002) Biochemistry 41, 14238-14247] [8].
  • Molecular modeling using coordinates for the recently determined N-terminal domain of human SBP revealed a significant shift of the F56 phenyl ring away from ring A of E(2) in mutant models containing the R140K and I141L replacements [10].
  • Bisulfite sequencing further verified a densely methylated pattern of 35 CpG sites studied in M1 that were not found in normal brain, indicating that inactivation of DLC-1 by hypermethylation is involved in SPNET [11].
  • We conclude that R140 and I141 are required for sustaining the right proximity of the phenyl ring of F56 to ring A of 17beta-estradiol, thus optimizing the E(2)-binding affinity of human SBP [10].
  • DLC-1 mRNA expression in cells with or without treatment with 5-aza-deoxycytidine (5-aza-CdR) or trichostatin A (TSA) was investigated by real-time RT-PCR [12].

Other interactions of DLEC1


Analytical, diagnostic and therapeutic context of DLEC1

  • By site-directed mutagenesis, we have identified several amino acid residues on cten and DLC-1 that are essential for this interaction [4].
  • The methylation of the candidate tumor suppressor gene DLC-1 was detected in a high proportion of primary tumor and plasma DNA samples by using quantitative methylation-specific PCR analysis [7].
  • METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect DLC-1 transcripts in RPMI 8226, U266, OPM-2 and XG-2 cell lines [12].


  1. MIRA-Assisted Microarray Analysis, a New Technology for the Determination of DNA Methylation Patterns, Identifies Frequent Methylation of Homeodomain-Containing Genes in Lung Cancer Cells. Rauch, T., Li, H., Wu, X., Pfeifer, G.P. Cancer Res. (2006) [Pubmed]
  2. Epigenetic inactivation of the deleted in lung and esophageal cancer 1 gene in nasopharyngeal carcinoma. Kwong, J., Chow, L.S., Wong, A.Y., Hung, W.K., Chung, G.T., To, K.F., Chan, F.L., Daigo, Y., Nakamura, Y., Huang, D.P., Lo, K.W. Genes Chromosomes Cancer (2007) [Pubmed]
  3. Candidate tumor-suppressor gene DLEC1 is frequently downregulated by promoter hypermethylation and histone hypoacetylation in human epithelial ovarian cancer. Kwong, J., Lee, J.Y., Wong, K.K., Zhou, X., Wong, D.T., Lo, K.W., Welch, W.R., Berkowitz, R.S., Mok, S.C. Neoplasia (2006) [Pubmed]
  4. The phosphotyrosine-independent interaction of DLC-1 and the SH2 domain of cten regulates focal adhesion localization and growth suppression activity of DLC-1. Liao, Y.C., Si, L., Devere White, R.W., Lo, S.H. J. Cell Biol. (2007) [Pubmed]
  5. Characterization of two Phaseolus vulgaris phytohemagglutinin genes closely linked on the chromosome. Hoffman, L.M., Donaldson, D.D. EMBO J. (1985) [Pubmed]
  6. Molecular cloning of a candidate tumor suppressor gene, DLC1, from chromosome 3p21.3. Daigo, Y., Nishiwaki, T., Kawasoe, T., Tamari, M., Tsuchiya, E., Nakamura, Y. Cancer Res. (1999) [Pubmed]
  7. Discovery of novel epigenetic markers in non-Hodgkin's lymphoma. Shi, H., Guo, J., Duff, D.J., Rahmatpanah, F., Chitima-Matsiga, R., Al-Kuhlani, M., Taylor, K.H., Sjahputera, O., Andreski, M., Wooldridge, J.E., Caldwell, C.W. Carcinogenesis (2007) [Pubmed]
  8. Influence of the dimer interface on glutathione transferase structure and dynamics revealed by amide H/D exchange mass spectrometry. Codreanu, S.G., Thompson, L.C., Hachey, D.L., Dirr, H.W., Armstrong, R.N. Biochemistry (2005) [Pubmed]
  9. Immunoglobulin superfamily receptor translocation associated 2 protein on lymphoma cell lines and hairy cell leukemia cells detected by novel monoclonal antibodies. Ise, T., Maeda, H., Santora, K., Xiang, L., Kreitman, R.J., Pastan, I., Nagata, S. Clin. Cancer Res. (2005) [Pubmed]
  10. Arginine-140 and isoleucine-141 determine the 17beta-estradiol-binding specificity of the sex-steroid-binding protein (SBP, or SHBG) of human plasma. Petra, P.H., Adman, E.T., Orr, W.R., Woodcock, K.T., Groff, C., Sui, L.M. Protein Sci. (2001) [Pubmed]
  11. Epigenetic inactivation of DLC-1 in supratentorial primitive neuroectodermal tumor. Pang, J.C., Chang, Q., Chung, Y.F., Teo, J.G., Poon, W.S., Zhou, L.F., Kong, X., Ng, H.K. Hum. Pathol. (2005) [Pubmed]
  12. High-frequency promoter hypermethylation of the deleted in liver cancer-1 gene in multiple myeloma. Song, Y.F., Xu, R., Zhang, X.H., Chen, B.B., Chen, Q., Chen, Y.M., Xie, Y. J. Clin. Pathol. (2006) [Pubmed]
  13. Deletion mapping using quantitative real-time PCR identifies two distinct 3p21.3 regions affected in most cervical carcinomas. Senchenko, V., Liu, J., Braga, E., Mazurenko, N., Loginov, W., Seryogin, Y., Bazov, I., Protopopov, A., Kisseljov, F.L., Kashuba, V., Lerman, M.I., Klein, G., Zabarovsky, E.R. Oncogene (2003) [Pubmed]
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