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Gene Review

FOSL1  -  FOS-like antigen 1

Homo sapiens

Synonyms: FRA, FRA-1, FRA1, Fos-related antigen 1, fra-1
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Disease relevance of FOSL1


High impact information on FOSL1


Chemical compound and disease context of FOSL1


Biological context of FOSL1


Anatomical context of FOSL1

  • Human T-cell leukemia virus type 1 Tax activates transcription of the human fra-1 gene through multiple cis elements responsive to transmembrane signals [14].
  • Ectopic Fra-1 induced prominent phenotypic changes in all three malignant glioma cell lines examined: H4, U-87 MG, and A-172 MG [4].
  • RPL38, FOSL1, and UPP1 are predominantly expressed in the pancreatic ductal epithelium [15].
  • Four proteins (FBR-v-Fos, FBJ-v-Fos, c-Fos, and FosB) transform established rodent fibroblast cell lines, while three (FosB2, Fra1, and Fra2) do not [16].
  • Moreover, induction of c-fos resulted in the concomitant increase in the expression of fra-1 and c-jun, further highlighting the importance of AP-1 transcription factors in chondrocyte differentiation [17].

Associations of FOSL1 with chemical compounds

  • As a further step, we have investigated whether bilberries and quercetin have the ability to induce transcription of Fos-related antigen 1 (Fra-1), which contains two EpREs in its promoter [18].
  • Thrombin but not carbachol also induces a late increase in fra-1 mRNA, which peaks at 12 h [19].
  • Treatment of cells with LY294002, an inhibitor of the PI3K-Akt pathway, completely blocked CS-induced FRA-1 expression [20].
  • Irrespective of enhanced c-fos expression, c-jun was phosphorylated and became primarily heterodimerized with fra-1, which was also induced after PDTC incubation [21].
  • Most interestingly, curcumin can reverse the expression dynamics of c-fos and fra-1 in this tumorigenic cell line, mimicking the expression pattern observed in normal controls or precancerous lesions [22].

Physical interactions of FOSL1


Regulatory relationships of FOSL1

  • In contrast, Fra-1 strongly inhibits inducible IL-8 transcription [25].
  • Analyses of AP-1 composition revealed that MCP-1 is only expressed in those cells where jun-family members were mainly heterodimerized with the fos-related protein fra-1 [26].
  • Overexpression of fra1 in malignant cells significantly enhanced SPRR1B promoter activity [27].
  • Transcription of the fos, fra-1 and fra-2 genes was induced by phorbol ester (TPA) stimulation of U937 human monocytic cells [28].
  • Members of the AP1 family distinctly regulated the fra-1 promoter [13].

Other interactions of FOSL1

  • Relative to c-Fos, the delayed recruitment of Fra-1 to the IL-8 promoter provides an example how AP-1 subunits may dampen excessive chemokine synthesis [25].
  • PMA significantly induced binding of JunB and Fra1 in normal cells, while JunB and Fra2 bound to TREs in the malignant cells [27].
  • In contrast, in tumorigenic cells the 1: 1 ratio between jun and fra-1 is disturbed and the MCP-1 gene is no longer expressed [26].
  • FRA-1, a member of the FOS family of transcription factors, is overexpressed in a variety of human tumors, and contributes to tumor progression [11].
  • Fra-1 activation involves its stabilization, ubiquitination, and interaction with histone deacetylase-1 [25].

Analytical, diagnostic and therapeutic context of FOSL1


  1. FRA-1 expression level regulates proliferation and invasiveness of breast cancer cells. Belguise, K., Kersual, N., Galtier, F., Chalbos, D. Oncogene (2005) [Pubmed]
  2. DNA-binding activity of Jun is increased through its interaction with Fos. Allegretto, E.A., Smeal, T., Angel, P., Spiegelman, B.M., Karin, M. J. Cell. Biochem. (1990) [Pubmed]
  3. Expression pattern of the AP-1 family in endometrial cancer: correlations with cell cycle regulators. Bamberger, A.M., Milde-Langosch, K., Rössing, E., Goemann, C., Löning, T. J. Cancer Res. Clin. Oncol. (2001) [Pubmed]
  4. Fos-related antigen 1 modulates malignant features of glioma cells. Debinski, W., Gibo, D.M. Mol. Cancer Res. (2005) [Pubmed]
  5. The product of a fos-related gene, fra-1, binds cooperatively to the AP-1 site with Jun: transcription factor AP-1 is comprised of multiple protein complexes. Cohen, D.R., Ferreira, P.C., Gentz, R., Franza, B.R., Curran, T. Genes Dev. (1989) [Pubmed]
  6. NMDA-Receptor Activation Induces Calpain-Mediated beta-Catenin Cleavages for Triggering Gene Expression. Abe, K., Takeichi, M. Neuron (2007) [Pubmed]
  7. Target genes of beta-catenin-T cell-factor/lymphoid-enhancer-factor signaling in human colorectal carcinomas. Mann, B., Gelos, M., Siedow, A., Hanski, M.L., Gratchev, A., Ilyas, M., Bodmer, W.F., Moyer, M.P., Riecken, E.O., Buhr, H.J., Hanski, C. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  8. Nrf1 and Nrf2 positively and c-Fos and Fra1 negatively regulate the human antioxidant response element-mediated expression of NAD(P)H:quinone oxidoreductase1 gene. Venugopal, R., Jaiswal, A.K. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  9. Increased c-fos mRNA expression by human fibroblasts contracting stressed collagen matrices. Rosenfeldt, H., Lee, D.J., Grinnell, F. Mol. Cell. Biol. (1998) [Pubmed]
  10. FRA-1 expression level modulates regulation of activator protein-1 activity by estradiol in breast cancer cells. Philips, A., Teyssier, C., Galtier, F., Rivier-Covas, C., Rey, J.M., Rochefort, H., Chalbos, D. Mol. Endocrinol. (1998) [Pubmed]
  11. Mitogen regulated induction of FRA-1 proto-oncogene is controlled by the transcription factors binding to both serum and TPA response elements. Adiseshaiah, P., Peddakama, S., Zhang, Q., Kalvakolanu, D.V., Reddy, S.P. Oncogene (2005) [Pubmed]
  12. Fra-1 a target for cancer prevention or intervention. Young, M.R., Colburn, N.H. Gene (2006) [Pubmed]
  13. Multiple cis-elements mediate the transcriptional activation of human fra-1 by 12-O-tetradecanoylphorbol-13-acetate in bronchial epithelial cells. Adiseshaiah, P., Papaiahgari, S.R., Vuong, H., Kalvakolanu, D.V., Reddy, S.P. J. Biol. Chem. (2003) [Pubmed]
  14. Human T-cell leukemia virus type 1 Tax activates transcription of the human fra-1 gene through multiple cis elements responsive to transmembrane signals. Tsuchiya, H., Fujii, M., Niki, T., Tokuhara, M., Matsui, M., Seiki, M. J. Virol. (1993) [Pubmed]
  15. RPL38, FOSL1, and UPP1 are predominantly expressed in the pancreatic ductal epithelium. Sahin, F., Qiu, W., Wilentz, R.E., Iacobuzio-Donahue, C.A., Grosmark, A., Su, G.H. Pancreas (2005) [Pubmed]
  16. Transformation by Fos proteins requires a C-terminal transactivation domain. Wisdon, R., Verma, I.M. Mol. Cell. Biol. (1993) [Pubmed]
  17. Inhibition of chondrocyte differentiation in vitro by constitutive and inducible overexpression of the c-fos proto-oncogene. Thomas, D.P., Sunters, A., Gentry, A., Grigoriadis, A.E. J. Cell. Sci. (2000) [Pubmed]
  18. Bilberry extracts induce gene expression through the electrophile response element. Myhrstad, M.C., Carlsen, H., Dahl, L.I., Ebihara, K., Glemmestad, L., Haffner, K., Moskaug, J.Ø., Blomhoff, R. Nutrition and cancer. (2006) [Pubmed]
  19. Biphasic increase in c-jun mRNA is required for induction of AP-1-mediated gene transcription: differential effects of muscarinic and thrombin receptor activation. Trejo, J., Chambard, J.C., Karin, M., Brown, J.H. Mol. Cell. Biol. (1992) [Pubmed]
  20. A Phosphatidylinositol 3-kinase-regulated Akt-independent signaling promotes cigarette smoke-induced FRA-1 expression. Zhang, Q., Adiseshaiah, P., Kalvakolanu, D.V., Reddy, S.P. J. Biol. Chem. (2006) [Pubmed]
  21. Antioxidant-induced changes of the AP-1 transcription complex are paralleled by a selective suppression of human papillomavirus transcription. Rösl, F., Das, B.C., Lengert, M., Geletneky, K., zur Hausen, H. J. Virol. (1997) [Pubmed]
  22. Constitutive activation of transcription factor AP-1 in cervical cancer and suppression of human papillomavirus (HPV) transcription and AP-1 activity in HeLa cells by curcumin. Prusty, B.K., Das, B.C. Int. J. Cancer (2005) [Pubmed]
  23. Transcription repressor activity of spleen tyrosine kinase mediates breast tumor suppression. Wang, L., Devarajan, E., He, J., Reddy, S.P., Dai, J.L. Cancer Res. (2005) [Pubmed]
  24. Proximal promoter of the surfactant protein D gene: regulatory roles of AP-1, forkhead box, and GT box binding proteins. He, Y., Crouch, E.C., Rust, K., Spaite, E., Brody, S.L. J. Biol. Chem. (2000) [Pubmed]
  25. MEK1-dependent delayed expression of Fos-related antigen-1 counteracts c-Fos and p65 NF-kappaB-mediated interleukin-8 transcription in response to cytokines or growth factors. Hoffmann, E., Thiefes, A., Buhrow, D., Dittrich-Breiholz, O., Schneider, H., Resch, K., Kracht, M. J. Biol. Chem. (2005) [Pubmed]
  26. Differential transcriptional regulation of the monocyte-chemoattractant protein-1 (MCP-1) gene in tumorigenic and non-tumorigenic HPV 18 positive cells: the role of the chromatin structure and AP-1 composition. Finzer, P., Soto, U., Delius, H., Patzelt, A., Coy, J.F., Poustka, A., zur Hausen, H., Rösl, F. Oncogene (2000) [Pubmed]
  27. Mechanism of repression of squamous differentiation marker, SPRR1B, in malignant bronchial epithelial cells: role of critical TRE-sites and its transacting factors. Patterson, T., Vuong, H., Liaw, Y.S., Wu, R., Kalvakolanu, D.V., Reddy, S.P. Oncogene (2001) [Pubmed]
  28. Isolation of human fos-related genes and their expression during monocyte-macrophage differentiation. Matsui, M., Tokuhara, M., Konuma, Y., Nomura, N., Ishizaki, R. Oncogene (1990) [Pubmed]
  29. Regulation of the urokinase-type plasminogen activator receptor gene in different grades of human glioma cell lines. Bhattacharya, A., Lakka, S.S., Mohanam, S., Boyd, D., Rao, J.S. Clin. Cancer Res. (2001) [Pubmed]
  30. Genetic complementation to non-tumorigenicity in cervical-carcinoma cells correlates with alterations in AP-1 composition. Soto, U., Denk, C., Finzer, P., Hutter, K.J., zur Hausen, H., Rösl, F. Int. J. Cancer (2000) [Pubmed]
  31. A novel retinoic acid receptor beta isoform and retinoid resistance in lung carcinogenesis. Petty, W.J., Li, N., Biddle, A., Bounds, R., Nitkin, C., Ma, Y., Dragnev, K.H., Freemantle, S.J., Dmitrovsky, E. J. Natl. Cancer Inst. (2005) [Pubmed]
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