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Siological conditions during tumor growth we sought evidence of TUSC2 hypoxic link. As a result, we found in the NCBI Gene Expression Omnibus several experimental assays performed on different cell types that consistently showed TUSC2 mRNA suppression by hypoxia (see records GDS2759, GDS2018, GDS2760, and GDS2951 for FUS1/TUSC2 at http:// www.ncbi.nlm.nih.gov/sites/entrez). Based on these data and
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Siological conditions during tumor growth we sought evidence of TUSC2 hypoxic link. As a result, we found in the NCBI Gene Expression Omnibus several experimental assays performed on different cell types that consistently showed TUSC2 mRNA suppression by hypoxia (see records GDS2759, GDS2018, GDS2760, and GDS2951 for FUS1/TUSC2 at http:// www.ncbi.nlm.nih.gov/sites/entrez). Based on these data and
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Y is consistent with the haploinsufficient effect of the gene observed in our mouse KO model. Indeed, mice hetero- or homozygous on the Tusc2 deletion shared similar immunological and tumorigenic phenotypes at comparable frequencies. These data suggest that even partial loss of the TUSC2 dosage is sufficient to trigger pathological inflammation and increase susceptibility to cancer [15]. We consid
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Arotene induced) 3 SELENBP1, selenium binding protein 1 SIDT2, SID1 transmembrane family, member 2 SAMD9L, sterile alpha motif domain containing 9-like TNS1, tensin+2.5 +2.4 +4.-2.6 -3.2 -2.+2.RGS4, regulator of G-protein signaling-4.+2.1 +2.3 +2.0 +2.SET, SET translocation (myeloid leukemia-associated) SKIL, SKI-like oncogene THBS1, thrombospondin 1 B4GALT1, UDP-Gal:betaGlcNAc beta 1,4galactosylt
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Arotene induced) 3 SELENBP1, selenium binding protein 1 SIDT2, SID1 transmembrane family, member 2 SAMD9L, sterile alpha motif domain containing 9-like TNS1, tensin+2.5 +2.4 +4.-2.6 -3.2 -2.+2.RGS4, regulator of G-protein signaling-4.+2.1 +2.3 +2.0 +2.SET, SET translocation (myeloid leukemia-associated) SKIL, SKI-like oncogene THBS1, thrombospondin 1 B4GALT1, UDP-Gal:betaGlcNAc beta 1,4galactosylt
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Box N3 zinc finger E-box binding homeobox 1 protocadherinRPS11 HIST1H2AE RGS4 PTHLH HIST1H2BG CD24 PSMB4 LOX PPP1R15A HIST1H4H ATF3 SET HIST2H2BE LOC284801 TMEM158 HIST2H2AA3 FBXO32 HIST1H3D SOX4 FEM1B BCL2L11 WSB1 C1orf21 MBNL1 SELENBP1 BTN3A1 AFF4 TMEM47 SOD2 SIDT2 TMCC1 EGR1 ALDH6A1 CCNG2 CDC2L6 RNASE4 TNS1 MLL5 FOXN3 ZEB1 PCDHPage 9 of(page number not for citation purposes)Molecular Cancer 200
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Tos effect. This observation suggests that the suppressive effect of asbestos on TUSC2 expression is mediated via ROS. Indeed, generation of ROS by asbestos was documented in many studies [25]. A yet another source of ROS that may keep the TUSC2 level down in normal and malignant tissues are inflammatory cells attracted to the site of asbestos lodging [31]. We previously showed that TUSC2 is expre
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Arotene induced) 3 SELENBP1, selenium binding protein 1 SIDT2, SID1 transmembrane family, member 2 SAMD9L, sterile alpha motif domain containing 9-like TNS1, tensin+2.5 +2.4 +4.-2.6 -3.2 -2.+2.RGS4, regulator of G-protein signaling-4.+2.1 +2.3 +2.0 +2.SET, SET translocation (myeloid leukemia-associated) SKIL, SKI-like oncogene THBS1, thrombospondin 1 B4GALT1, UDP-Gal:betaGlcNAc beta 1,4galactosylt