RETRACTED ARTICLE: TIPE2 suppresses progression and tumorigenesis of esophageal carcinoma via inhibition of the Wnt/β-catenin pathway
Male
Esophageal Neoplasms
Carcinogenesis
Proliferation
Down-Regulation
Mice, Nude
Apoptosis
03 medical and health sciences
Cell Line, Tumor
Wnt/β-catenin pathway
Animals
Humans
Neoplasm Invasiveness
Wnt Signaling Pathway
Aged
Cell Proliferation
Mice, Inbred BALB C
0303 health sciences
Research
R
Intracellular Signaling Peptides and Proteins
Middle Aged
Xenograft Model Antitumor Assays
TIPE2
3. Good health
Gene Expression Regulation, Neoplastic
Esophageal carcinoma
Tumorigenesis
Disease Progression
Medicine
Female
DOI:
10.1186/s12967-018-1383-0
Publication Date:
2018-01-17T12:25:08Z
AUTHORS (16)
ABSTRACT
Abstract
Background
Esophageal carcinoma is the eighth prevalent malignancy and ranks the sixth in carcinoma-related death worldwide. Tumor necrosis factor-α-induced protein-8 like-2 (TIPE2) has been identified as a tumor suppressor in multiple carcinomas. However, its roles and molecular mechanisms underlying esophageal carcinoma progression are still undefined till now.
Methods
RT-qPCR assay was employed to detect the expression of TIPE2 mRNA. TIPE2 protein expression was measured by using western blot assay. Ad-V and Ad-TIPE2 adenoviruses were constructed to overexpress TIPE2. The effects of TIPE2 overexpression on cell proliferation, invasion and apoptosis were assessed by MTT and Edu incorporation assays, transwell invasion assay and flow cytometry analysis, respectively. The effect of TIPE2 overexpression on xenograft tumor growth was determined by measuring tumor volume and weight, together with immunohistochemistry assay. The effect of TIPE2 overexpression on the Wnt/β-catenin signaling pathway was evaluated by detecting the protein levels of β-catenin, c-Myc and cyclinD1 in EC9076 cells and xenograft tumors of esophageal carcinoma.
Results
TIPE2 expression was downregulated in esophageal carcinoma tissues and cells. Adenovirus-mediated TIPE2 overexpression suppressed cell proliferation and invasion, and induced apoptosis in esophageal carcinoma cells. Enforced expression of TIPE2 inhibited tumor growth in vivo, as evidenced by the reduced tumor volume, tumor weight and proliferating cell nuclear antigen expression. Overexpression of TIPE2 inhibited the Wnt/β-catenin signaling pathway in esophageal carcinoma in vitro and in vivo.
Conclusions
These results suggest that TIPE2 suppressed progression and tumorigenesis of esophageal carcinoma via inhibition of the Wnt/β-catenin pathway.
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CITATIONS (21)
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