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Tumor Discovery                                                 CK2 deregulation in non-small-cell lung cancer




                        A                                  B























                                                           C

























            Figure 4.  Correlation of CSNK2A1 gene expression levels with infiltrating cell populations in the tumor microenvironment, as analyzed using the TIMER2.0
            database. (A) Correlations were assessed using four metrics for cancer-associated fibroblasts (CAFs) (CAF_EPIC, CAF_MCPCOUNTER, CAF_XCELL,
            CAF_TIDE) and one for myeloid-derived suppressor cells (MDCS) (MDSC_TIDE) across TCGA tumor types; “n” denotes the numbers of clinical samples
            within each cohort; (B) Detailed correlation analysis of CAF infiltration (CAF_TIDE metric) with CSNK2A1 expression level (Log2- TPM) in LUAD and
            LUSC; (C) Detailed analysis of MDSC infiltration (MDSC_TIDE metric) with CSNK2A1 expression level (Log2-TPM) in LUAD and LUSC. Each analysis was
            normalized for sample purity, with significant correlations indicated by color-filled boxes in the heatmap, where color intensity reflects correlation strength.
            Abbreviations: CAF: Cancer-associated fibroblasts; TPM: transcripts per million; LUAD: lung adenocarcinoma; LUSC: lung squamous carcinoma.

            correlations with each other, particularly in LUSC samples   parallel, several CK2 inhibitors have been developed and
            (R = 0.683), whereas CSNK2B positively correlated only   tested for antineoplastic effects in both in vitro and in vivo.
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            with CSNK2A1 in LUAD (R = 0.372) (Table S6).       Despite this wealth of information and the availability of
                                                               therapeutic compounds targeting CK2, only two CK2
            4. Discussion                                      inhibitors have advanced to clinical trials. 11,12
            The  deregulation of CK2  and  its  potential  role  in   Notably, translational and clinical data on CK2 remain
            neoplastic processes have been revisited in recent   relatively limited and sparse.  In a pioneering study,
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            studies.  CK2 enzyme biochemistry, aberrant expression,   Ortega  et al.  analyzed  CSNK2 transcript expression
                  24
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            phosphorylation cascades, and the enzyme’s tumor-  in seven tumor types, including lung cancers, using
            supportive activities – both intrinsic and extrinsic – have   the Oncomine database.  CSNK2A1,  CSNK2A2, and
            been extensively investigated in preclinical models. 13,25  In   CSNKB mRNA transcripts were overexpressed in 14/14,
            Volume 3 Issue 4 (2024)                         8                                 doi: 10.36922/td.4571
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