Background: The most common cancer among humans is lung cancer. Non-small cell lung cancer (NSCLC) comprises the majority of these cases. In the development and progression of cancers across the spectrum, tumor abnormal protein (TAP) plays crucial roles. Additionally, in the advancement of the bladder and colorectal cancers, the involvement of glycoproteins like TAP is present. However, it is worth noting that current literature has yet to clarify the clinical significance of the TAP in NSCLC. Methods: In the present study, to evaluate the relative level of TAP, we utilized a TAP detection agent in 154 cases of NSCLC and normal patients who underwent surgical resection anytime from March 2013 to January 2019 at the People's Hospital of Chizhou. Results: Our results demonstrated that in NSCLC patients, the expression level of TAP was significantly higher than in normal patients. Moreover, after surgery, TAP expression was significantly downregulated in NSCLC patients. TAP expression is associated with an array of factors, which include the patient's sex, history of smoking use, tumor size, pTNM, distant cancer, metastasis of lymph nodes, invasive and aggressive indicator pleural invasion, and differentiation degree of NSCLC. Additionally, TAP has no association with the patient's age, history of drinking, location of the tumor, hypertension, and diabetes. In NSCLC patients, a poor overall survival rate within 5 years is significantly correlated with the increased TAP expression. For NSCLC patients, an independent prognostic factor is the TAP, which is confirmed using the multivariate survival analysis. Conclusion: In the malignant progression of NSCLC, our results demonstrate how the promoting role of the upregulated TAP expression takes place. Hence, a therapeutic aim for NSCLC and a potential biomarker for NSCLC progress is a TAP.

Background: Esophageal squamous cell carcinoma (ESCC) acts as a fatal malignant tumor among human beings and is marked by late-stage diagnosis, frequent recurrence, metastasis, and therapy resistance. Tumor abnormal protein (TAP) remarkably affects cancer development and progression of human cancers. TAP has been shown to be a biomarker for gastric and lung cancer progression. Nevertheless, the clinical value exhibited by TAP for ESCC has not been well-explained in the current literature.Methods: The present study included 183 ESCC cases who received surgical resection and 183 cases who had normal physical checkup from March 2013 to January 2015 at the People's Hospital of Chizhou, and used the TAP detection agent for evaluating the TAP relative level.Results: As found, ESCC patients presented an obviously higher TAP expression relative to cases who had normal physical checkup. Moreover, TAP expression was significantly downregulated after surgery. Furthermore, the TAP expression was correlated with gender, smoking, pathologic differentiation, and pN stage, but not with age, tumor location, surgical type, pT stage, and vascular invasion. High expression of TAP was significantly correlated with poorer overall survival (OS) rate in ESCC patients. TAP was an independent prognostic predictor in ESCC patients, based on the multivariate survival analysis.Conclusion: The study reveals how TAP upregulation promotes ESCC malignant progression, and concludes that TAP acts as the therapeutic target and potential biomarker specific to ESCC.

Lung adenocarcinoma (LUAD) remains a major reason of cancer-associated mortality globally, and there exists a lack of indicators for survival in LUAD patients. Therefore, it is clinically required to obtain a novel prognostically indicator for guiding clinical management. In this study, we established a circadian rhythm (CR) related signature by a combinative investigation of multiple datasets. The newly-established signature showed an acceptable ability to predict survival and could serve as an independent indicator for prognosis. Moreover, the newly-established signature was critically associated with tumor malignancy, including proliferation, invasion, EMT and metastasis. The newly-established signature was predictive of response to immune checkpoint blockade. Collectively, we established a CR-related gene signature that could forecast survival, tumor malignancy and therapeutic response; our findings could help guiding clinical management.

To identify a cancer stemness-related prognostic signature, we analyzed RNA-seq data of patients with lung adenocarcinoma from the TCGA and GEO cohort using univariate Cox and LASSO analysis. Eight genes (PLEK2, GPX8, TCN1, PERP, CD79A, PAX5, FSCN1, and CNNM1) were eventually identified to develop a cancer stemness-related signature. AUCs for 5-year overall survival were 0.681, 0.673, and 0.774 in the training, validation, and test sets, respectively. Kaplan-Meier curve analysis showed that the high-risk group has a poor survival as compared with the low-risk group in the training set, validation set, and test set, respectively (P < 0.05). Six genes (PLEK2, GPX8, TCN1, PERP, FSCN1, and CNNM1) were significantly upregulated in the cancerous tissue compared with in the normal tissue (P < 0.001), and correlated with an unwanted prognosis (P < 0.05). We constructed a prognostic nomogram combining the cancer stemness-related signature with TNM staging to precisely assess the prognosis of the patient with lung adenocarcinoma. Finally, we observed that the stemness-related gene signature also could predict the malignant levels of lung adenocarcinoma possibly via hypoxia, epithelial-mesenchymal transition and angiogenesis. Conclusively, this study developed a novel cancer stemness-related gene signature, and identified six pivotal genes which can serve as potential therapeutic targets in the treatment of lung cancer.