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Expression analysis of TRAF2‑ and NCK‑interacting protein kinase (TNIK) and phosphorylated TNIK in papillary thyroid
Jiali Li1, Lili Lan2, Yuru Xu2
1Research Center, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China.
Abstract:
The aim of the present study was to evaluate the expression of TRAF2- and NCK-interacting kinase (TNIK) and the levels of the active form of TNIK, phosphorylated (p)-TNIK, in papillary thyroid carcinoma (PTC), and to identify and compare the levels of TNIK and p-TNIK among PTC, benign thyroid tumors and normal tissues. The levels of TNIK and p-TNIK were examined by reverse transcription-quantitative (RT-q)PCR and immunohistochemical analysis (IHC) in PTC, benign thyroid tumors and normal tissues, and their association with clinicopathological features was evaluated. First, analysis of the Gene Expression Profiling Interactive Analysis and The Cancer Genome Atlas datasets suggested that the mRNA expression of TNIK was markedly increased in PTC tissues compared with that in normal tissues. RT-qPCR analyses then indicated that the relative mRNA expression of TNIK in PTC tissues was 4.47±6.16, which was significantly higher than that in adjacent tissues 2.57±5.83. The IHC results suggested that the levels of TNIK and p-TNIK in PTC tissues were markedly elevated compared with those in benign thyroid tumors and normal tissues. The levels of p-TNIK in patients with PTC were significantly associated with extrathyroidal extension (χ2=4.199, P=0.040). Positive staining for TNIK was observed in 187 out of 202 (92.6%) cases in the cytoplasm, nucleus or cytomembrane of PTC cells. Among the 187 positive cases, cytoplasm expression was identified in 162 cases (86.6%), nuclear expression in 17 cases (9.1%) and cytomembrane expression in 8 cases (4.3%). Positive staining for p-TNIK was observed in 179 out of 202 (88.6%) cases in the nuclei, cytoplasm or cytomembrane of PTC cells. In the 179 p-TNIK-positive cases, localization in the nuclei plus cytoplasm was identified in 142 cases (79.3%), nuclear localization in 9 cases (5.0%), presence in the cytoplasm in 21 cases (11.7%) and cytomembrane localization in 7 cases (3.9%). Both TNIK and p-TNIK were upregulated in PTC tissues and p-TNIK was significantly associated with extrathyroidal extension. It may act as a crucial oncogene to participate in PTC carcinogenesis and progression.
Insights
TRAF2- and NCK-interacting kinase (TNIK) and its active form, p-TNIK, are significantly upregulated in papillary thyroid carcinoma (PTC). Elevated p-TNIK levels correlate with extrathyroidal extension, suggesting TNIK
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer.
- Understanding the molecular mechanisms underlying PTC development and progression is crucial for effective treatment strategies.
Purpose of the Study:
- To evaluate the expression of TNIK and p-TNIK in PTC tissues.
- To compare TNIK and p-TNIK levels in PTC, benign thyroid tumors, and normal tissues.
- To investigate the association between TNIK/p-TNIK levels and clinicopathological features in PTC.
Main Methods:
- Analysis of Gene Expression Profiling Interactive Analysis and The Cancer Genome Atlas datasets for TNIK mRNA expression.
- Reverse transcription-quantitative PCR (RT-qPCR) to quantify TNIK mRNA levels.
- Immunohistochemical analysis (IHC) to assess TNIK and p-TNIK protein expression and localization.
Main Results:
- TNIK mRNA expression was significantly increased in PTC tissues compared to normal tissues.
- Both TNIK and p-TNIK protein levels were markedly elevated in PTC tissues compared to benign thyroid tumors and normal tissues.
- Elevated p-TNIK levels were significantly associated with extrathyroidal extension in PTC patients.
Conclusions:
- TNIK and p-TNIK are upregulated in PTC.
- p-TNIK may play a crucial role as an oncogene in PTC carcinogenesis and progression.
- TNIK and p-TNIK are potential diagnostic and prognostic biomarkers for PTC.
