TNFAIP8 overexpression: a potential predictor of lymphatic metastatic recurrence in pN0 esophageal squamous cell carcinoma after Ivor Lewis esophagectomy

Sun, Zhenguo; Liu, Xiangyan; Song, Jee Hoon; Cheng, Yulan; Liu, Yü; Jia, Yongsheng; Meltzer, Stephen J.; Wang, Zhou

doi:10.1007/s13277-016-4978-1

Cited by 21 publications

(25 citation statements)

References 31 publications

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“…TIPE overexpression is also associated with lymph node metastasis and poor prognosis in intestinal-type gastric adenocarcinoma [40]. TIPE is a potential predictor of lymph node metastasis in pN0 esophageal squamous cell carcinoma after Ivor Lewis esophagectomy [41]. TIPE promotes the metastasis of non-small-cell lung cancer, mediates cisplatin resistance and can be used as a predictor of poor prognosis [42].…”

Section: Discussionmentioning

confidence: 99%

TIPE regulates VEGFR2 expression and promotes angiogenesis in colorectal cancer

Zhong

Qiu

et al. 2020

Int. J. Biol. Sci.

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Background: Metastasis is the leading cause of death in colorectal cancer (CRC) patients. It is regulated mainly by tumor cell angiogenesis, and angiogenesis is caused by the binding of vascular endothelial growth factor (VEGF) to vascular endothelial growth factor receptor 2 (VEGFR2). Tumor necrosis factor--induced protein 8 (TNFAIP8, hereto after TIPE) plays an important role in tumorigenesis, development, and prognosis. However, the relationship between TIPE and VEGFR2 in CRC angiogenesis and the mechanism of action remain unknown. Method: In this study, we used quantitative real-time PCR, Western blotting and immunohistochemistry to detect TIPE and VEGFR2 expression in 55 specimens from CRC patients. We also used HCT116 CRC cells and human umbilical vein endothelial cells (HUVECs) for in vitro experiments by stably transducing shTIPE and shRNA control lentivirus into HCT116 cells, detecting VEGFR2 expression after TIPE knockdown and repurposing the culture supernatant as conditioned medium to stimulate angiogenesis of HUVECs. In vivo experiments with chicken chorioallantoic membranes (CAMs) and a nude mouse matrix subcutaneous tumor model were performed to validate the effects of TIPE on angiogenesis. Additionally, we analyzed the expression and phosphorylation levels of PDK1 and blocked PDK1 expression using inhibitors to determine whether TIPE-induced changes in VEGFR2-mediated angiogenesis acted via the PI3K-Akt pathway. Results: We found that TIPE and VEGFR2 are highly expressed in CRC and act as oncogenes. TIPE knockdown also downregulated VEGFR2 expression, which resulted in simultaneous inhibition of cell proliferation, cell migration and angiogenesis. Then, in vivo experiments further demonstrated that TIPE promotes angiogenesis in CRC. Finally, we found that TIPE promotes VEGFR2-mediated angiogenesis by upregulating PDK1 expression and phosphorylation and that blocking PDK1 expression can inhibit this process. Conclusion: TIPE promotes angiogenesis in CRC by regulating the expression of VEGFR2, which may be a target for antiangiogenic cancer therapy.

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Section: Discussionmentioning

confidence: 99%

TIPE regulates VEGFR2 expression and promotes angiogenesis in colorectal cancer

Zhong

Qiu

et al. 2020

Int. J. Biol. Sci.

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“…76 Recently, many studies on Chinese population suggested that TNFAIP8 expression was related to other tumors such as thyroid papillary carcinoma, epithelial ovarian cancer, gastric cancer and esophageal squamous cell carcinoma. 42,45,47,[77][78][79][80] A study showed that TNFAIP8 overexpression was not obviously related with the prognosis of gastric cancer patients, but it was an independent prognostic factor for disease-free survival (DFS) and overall survival (OS) in patients with intestinal type of gastric cancer. 49 Recent studies related to TNFAIP8 and gastric cancer had focused on miRNAs, and it was well known that abnormal regulation of miRNAs could affect proliferation, apoptosis, invasion and metastasis in the development of tumors.…”

Section: Tnfaip8 and Malignant Tumorsmentioning

confidence: 99%

<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

Guo¹,

Yuan²

2020

OTT

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Tumor necrosis factor (TNF) is the first cytokine used in tumor biotherapy, but TNFrelated drugs are limited by the lack of specific targets. Tumor necrosis factor alpha-induced proteins (TNFAIPs), derived from TNF, is a protein family and participates in proliferation, invasion and metastasis of tumor cells. In order to better understand biological functions and potential roles of TNFAIPs in malignant tumors, this paper in the form of "Gene-Protein-Tumor correlation" summarizes the biological characteristics, physiological functions and mechanisms of TNFAIPs by searching National Center of Biotechnology Information, GeneCards, UniProt and STRING databases. The relationship between TNFAIPs and malignant tumors is analyzed, and protein-protein interaction diagram in members of TNFAIPs is drawn based on TNF for the first time. We find that TNF as a key factor is related to TNFAIP1, TNFAIP3, TNFAIP5, TNFAIP6, TNFAIP8 and TNFAIP9, which can be directly involved in activating TNFAIP1, TNFAIP5, TNFAIP8 and TNFAIP9. We confirm that the mechanism of TNFAIP1, TNFAIP2 and TNFAIP3 inducing tumors may be related to NF-κB signaling pathway, but the mechanism of tumor induction by other members of TNFAIPs is not clear. In the future, translational studies are needed to explore the mechanisms of TNF-TNFAIPs-tumors.

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“…These results make TNFAIP8 a candidate therapeutic target in colon cancer 42 . In esophageal squamous cell carcinoma, TNFAIP8 expression was correlated to tumor's TNM stage, metastatic ability, prognostic situations as well as the lymphoid system relapse after Ivor Lewis esophagectomy 43 , 44 .…”

Section: Tnfaip8 and Malignant Diseasesmentioning

confidence: 99%

Tumor Necrosis Factor-α Induced Protein 8: Pathophysiology, Clinical Significance, and Regulatory Mechanism

et al. 2018

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Tumor necrosis factor-α-induced protein-8 (TNFAIP8) is the earliest discovered component of TNFAIP8 family [tumor necrosis factor-α-induced protein-8 like (TIPE) family]. TNFAIP8 contains a putative death effector domain (DED) homologous to DED II in FLIP (Fas-associated death domain-like interleukin-1β-converting enzyme-inhibitory protein), which may affect cell survival/death process. Recently, it has been demonstrated that TNFAIP8 could inhibit apoptosis and autophagy in various types of cells. Moreover, TNFAIP8 level fluctuated evidently in patients with inflammatory, malignant, and autoimmune diseases, indicating that it might be an anti-apoptotic and oncogenetic protein. Herein we will review the discovery, gene/protein structure, pathophysiological functions, and clinical significance of TNFAIP8 together with its potential regulatory mechanism.

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TNFAIP8 overexpression: a potential predictor of lymphatic metastatic recurrence in pN0 esophageal squamous cell carcinoma after Ivor Lewis esophagectomy

Cited by 21 publications

References 31 publications

TIPE regulates VEGFR2 expression and promotes angiogenesis in colorectal cancer

TIPE regulates VEGFR2 expression and promotes angiogenesis in colorectal cancer

<p>Tumor Necrosis Factor Alpha-Induced Proteins in Malignant Tumors: Progress and Prospects</p>

Tumor Necrosis Factor-α Induced Protein 8: Pathophysiology, Clinical Significance, and Regulatory Mechanism

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