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

carcinoma, liver hepatocellular carcinoma, LUAD, LUSC, tumor size, invasion depth (T stage), and lymph node
pancreatic adenocarcinoma, prostate adenocarcinoma, metastasis. At the time of specimen collection, patients
pheochromocytoma and paraganglioma, rectal had not undergone radiotherapy and displayed no other
adenocarcinoma, sarcoma, skin cutaneous melanoma, systemic primary tumors besides NSCLC. Post-operative
thyroid carcinoma, thymoma, stomach adenocarcinoma, hematoxylin and eosin sections confirmed diagnoses of
and uterine corpus endometrial carcinoma. LUAD or LUSC.

2.3. Survival meta-analysis of CSNK2 genes in NSCLC IHC analysis was performed using primary antibodies
against CSNK2A1 (Ab76040, Abcam, USA), CSNK2A2
A survival meta-analysis for each CSNK2 gene was (#PA5-109601, Invitrogen, USA), CSNK2B (Ab#76025,
interrogated using the LUAD or LUSC subtype explorer Abcam, USA), AKT (CST#4691, Cell Signaling Technology,
database (https://lce.biohpc.swmed.edu/lungcancer/index. USA), AKTs129 (#BS-5188R, Bioss, USA), NPM1 (ab52644,
php#about). Output values were displayed based on all Abcam, USA), NPM1s125 (ab109546, Abcam, USA), and
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curated studies available. Ki67 (RMA-0542 WWW, Fuzhou Maishin Biotechnology,
2.4. Metastasis potential of CSNK2 genes in NSCLC China), following the immunohistochemical SP method
with the Fuzhou Maishin Ultrasensitive SP (Mouse/
Differential expression analysis of CSNK2 genes in tumor, Rabbit) IHC Kit (Fuzhou Maishin Biotechnology, China).
normal, and metastatic tissues was carried out using the A combined immunoreactivity score (CIS) was calculated
TNMplot database (https://tnmplot.com/analysis/). The based on signal intensity (scored from “0” for non-stained
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statistical method was set automatically to the Kruskal– to “3” for strong brown staining) and the frequency of
Wallis one-way non-parametric test. positive cells (from <5% = 0 points to >75% = 4 points)

2.5. Correlation of CSNK2 genes with immune in tumor samples. Each section analyzed was selected
infiltration randomly from the upper, lower, left, right, and central
regions of a magnified field (×400) to ensure representative
The gene module from the TIMER2.0 web server interpretation. The combined scores (A×B) were classified
(http://timer.cistrome.org) was used to select genes of as follows:
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interest (CSNK2 subunits) and visualize the correlation • Score 1 – 3: − (negative)
between their expression levels and the immune and • Score 4 – 5: + (weak positive)
stromal cell populations infiltrating tumor samples from • Score 6 – 7: ++ (positive)
TCGA. Immune infiltrate abundances were estimated • Score ≥8: +++ (strong positive)
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using multiple immune deconvolution methods,
including Tumor Immune Dysfunction and Exclusion 2.7. Statistical analysis
(TIDE), Microenvironment Cell Populations-counter Statistical analysis of IHC experiments was performed
(MCPCounter), Estimating the Proportion of Immune using the Statistical Package for the Social Sciences 27.0.
and Cancer cells (EPIC), and xCell. The generated heatmap Chi-squared tests and Fisher’s exact tests were used to
shows purity-adjusted Spearman’s rho correlations across analyze correlations. A two-sided P < 0.05 was considered
various cancer types. statistically significant for all calculations.
2.6. Immunohistochemical analysis of LUAD and 3. Results
LUSC specimens
A total of 134 pairs of wax blocks were prepared from 3.1. Mutational burden of CSNK2 subunits across
primary tumor specimens (LUAD = 103; LUSC = 31) cancer cohorts
and corresponding para-neoplastic tissue (>5 cm from Deregulation of CK2 in cancer is regarded as an example
the tumor) collected from patients initially diagnosed at of non-oncogene addition. To explore genetic alterations
the First Affiliated Hospital of South China University in CSNK2 genes that may contribute to aberrant kinase
(Hunan, China) since December 2021. This study was activity, we analyzed available cancer genomics databases.
approved by the Medical Ethics Committee of Nanhua Figure 1A illustrates that the genetic alteration rates for
University Affiliated First Hospital, Issuance, Review CSNK2A1, CSNK2A2, and CSNK2B in a pan-cancer cohort
Batch Number: 2021LL0115001, Meeting Date: January were 7%, 1.8%, and 6%, respectively. Most alterations were
15, 2021. Reviewed materials included the Research Plan CNA, while missense, splice site, and truncating mutations
Version YJFA20210114 and the Informed Consent Form were below 0.3%. Notably, these uncommon mutations did
Version ZQTY20210114. Clinical and pathological records not exhibit oncogenic potential based on their frequency,
provided data on patient age, sex, histological grade, distribution, and functional impact, as determined by

Volume 3 Issue 4 (2024) 3 doi: 10.36922/td.4571