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Mon cancers helps tumor progression contributing to evasion from immune surveillance [39]. Our data suggest that TUSC2 is a potent suppressor of this key immunoreceptor (Table 3 and Fig. 3). Since blocking of CD274 is now actively pursued as a novel immunotherapy [40,41], we suggest that TUSC2 may also have important immunotherapeutic implications. Our study on the TUSC2 role in mesothelioma under
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Binding domain in the TUSC2 molecule makes it possible to further analyze its transcriptional activities through mutational analysis. The similarity between TUSC2 and IRF7 is especially important since this IFNactivated transcriptional factor is a principal component of the anti-viral response initiated in mitochondria [42,43]. Since TUSC2 is a mitochondrial protein, our findings support an import
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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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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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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