Open AccessTNK2 promoted esophageal cancer progression via activating egfr‐akt signaling
Author(s) -
Zhang Anqing,
Zhang Rongxin,
Yang Zhiming,
Tian Rui
Publication year - 2021
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23700
Subject(s) - esophageal cancer , immunohistochemistry , western blot , medicine , cancer , protein kinase b , oncology , metastasis , cancer research , carcinoma , pathology , signal transduction , biology , gene , biochemistry
Background This study investigated the clinical implication of TNK2 expression in esophageal cancer patients’ cancer tissue samples. Methods The expression of TNK2 in esophageal cancer tissues and para‐carcinoma tissue was assessed with immunohistochemistry and Western blot analysis; besides, the proteins of CDC42, EGFR, and Akt were also analyzed. Then, Kaplan‐Meier survival curves of TNK2 protein expression level were assayed with 184 esophageal cancer patients from TCGA database. Moreover, with multiple linear regression analysis, we detected the correlations of TNK2 expression associated with tumor differentiation degree and metastasis status. Results It revealed that TNK2 was highly expressed in the cytoplasm of esophageal cancer tissues compared with para‐carcinoma tissue; besides, the proteins of CDC42, EGFR, and Akt were also up‐regulated in different levels of esophageal cancer tissues. However, there was no significant difference of the overall survival time of TNK2 protein expression in 184 esophageal cancer patients from TCGA database ( p = 0.37). But, in the included study samples of our study, there was positive coefficience between TNK2 protein expression and differentiation degree in esophageal cancer with multiple linear regression analysis [ R = 0.928, 95% confidence interval (0.085‐0.12)]. Conclusion Our results indicated that TNK2 was a potential diagnostic marker and promoted esophageal cancer progression through activating EGFR‐AKT signaling.