Disease relevance of Btg2

• Differential expression of TIS21 and TIS1 genes in the various organs of Balb/c mice, thymic carcinoma tissues and human cancer cell lines [1].
• Interestingly, induction of TIS21 expression was obliterated in the human lung cancer cells; A549 cells completely lost the ability to express TIS21 after a combined treatment of TPA and cycloheximide [1].

High impact information on Btg2

• Here we use mouse embryos expressing GFP from the Tis21 locus, a gene expressed throughout the neural tube in most, if not all, neuron-generating progenitors, to specifically reveal the cell divisions that produce CNS neurons [2].
• To demonstrate RNAi of endogenous gene expression, we used heterozygous embryos of a knock-in mouse line expressing GFP from the Tis21 locus, a gene turned on in neuroepithelial cells that switch from proliferation to neurogenesis [3].
• Transfection of a mouse Tis21 cDNA into the CHO-GD3-OAc(-) mutant cells restored 9-O-acetyl-GD3 expression [4].
• The four CHO mRNAs showing major up-regulation were homologous to VCAM-1, Tis21, the KC-protein-like protein, and a functionally unknown type II transmembrane protein [4].
• Genes modulated by expression of GD3 synthase in Chinese hamster ovary cells. Evidence that the Tis21 gene is involved in the induction of GD3 9-O-acetylation [4].

Biological context of Btg2

• The TIS21 immediate-early gene and leukemia-associated BTG1 gene encode proteins with similar sequences [5].
• Preferential induction by multiple promoters of these TIS genes in P-cells and enhancement of their induction in P+ cells by the anti-promoter forskolin make TIS1 and TIS21 candidates for promotion suppressor genes [6].
• As an endogenous cell death molecule, TIS21 may be involved in translocation of Pin-1 to cytoplasm [7].
• Potential roles of TIS21 have been suggested as transcriptional co-regulator, differentiation and antiapoptotic factor in neurogenesis, key mediator of the stage-specific expansion of thymocyte and negative regulator of hematopoietic progenitor expansion, and tumor suppressor gene in both mouse and human [7].
• Based on the previous report that the expression of TIS21 is involved in the induction of senescence after chemotherapy of cancer cells, which can be a mechanism to resist carcinogenesis, TIS21(/BTG2/PC3), the endogenous cell death molecule and pan-cell cycle regulator, might be a link between cellular senescence and carcinogenesis [7].

Anatomical context of Btg2

• Expression of TIS21 and TIS1 in the Balb/c mice thymus, lung, stomach and spleen was very strong (Lim IK et al. 1994a), regardless of TPA injection [1].
• In vivo induction of the TIS genes (TIS21, -8 and -1) by intraperitoneal injection of TPA was dramatic only at the needle contact site, i.e. in the abdominal muscle, not in the thigh muscle [1].
• The anti-proliferative gene TIS21 is involved in osteoclast differentiation [8].
• The TIS21 mRNA level was higher in differentiated-osteoclasts when compared to undifferentiated bone-marrow macrophages [8].
• On the other hand, it has lately been found that the expression of TIS21 is constitutive and high in thymus, lung alveolar epithelium, proximal tubule of kidney and basal cell layer of prostate acini [7].

Regulatory relationships of Btg2

• These data may suggest a repressed expression of TIS21 and TIS1 in the cancer tissues and cells derived from the organs that constitutively express TIS21 in mice and in human cancer cells [1].

Other interactions of Btg2

• Thymic carcinoma tissues developed in SV40-T-antigen-containing transgenic mice did not express TIS21 and TIS1, and expressed TIS8 weakly [1].
• The data showed that tis11, tis21, and junB early response genes were rapidly activated following IL-11 treatment [9].

Analytical, diagnostic and therapeutic context of Btg2

• To verify the cDNA microarray results, we carried out RT-PCR and real-time RT-PCR for the TIS21 gene [8].

References