NDLI: TRIM44 promotes human esophageal cancer progression via the AKT/mTOR pathway

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TRIM44 promotes human esophageal cancer progression via the AKT/mTOR pathway

Content Provider	Semantic Scholar
Author	Xiong, Dian Zhang Jin, Chun Ri Ye, Xudong Qiu, Baiquan Jianjun, Xu Zhu, Shuqiang Xiang, Long Cheng Wu, Haibo Yongbing, Wu
Copyright Year	2018
Abstract	Aberrant expression of TRIM-containing protein 44 (TRIM44) acts as a promoter in multiple cancers. Here, we investigated the biological functions and clinical significance of TRIM44 in human esophageal cancer (HEC). TRIM44 expression was significantly higher in HEC tissues than corresponding normal tissues at both the mRNA (2.42 ± 0.52 vs 0.99 ± 0.25) and protein (1.01 ± 0.27 vs 0.30 ± 0.13) levels. Patients with high TRIM44 expression showed poor differentiation (P = 1.39 × 10-5 ), advanced TNM stage (P = 3.87 × 10-4 ) and, most importantly, significantly poorer prognosis (P = 2.80 × 10-5 ). TRIM44 played a crucial role in epithelial mesenchymal transition (EMT). A significant correlation was observed between TRIM44 and Ki67 expression. We demonstrated that TRIM44 markedly enhanced HEC cell proliferation, migration, and invasion. Additionally, TRIM44 was involved in the AKT/mTOR signaling pathway and its downstream targets, such as STAT3 phosphorylation. Thus, elevated TRIM44 expression promotes HEC development by EMT via the AKT/mTOR pathway, and TRIM44 may be a novel prognostic indicator for HEC patients after curative resection.
Starting Page	3080
Ending Page	3092
Page Count	13
File Format	PDF HTM / HTML
PubMed reference number	30098109v1
Alternate Webpage(s)	https://doi.org/10.1111/cas.13762
DOI	10.1111/cas.13762
Journal	Cancer science
Volume Number	109
Language	English
Access Restriction	Open
Subject Keyword	Body tissue Cell Proliferation Esophageal carcinoma Excision FRAP1 protein, human Neoplasms Patients Proto-Oncogene Proteins c-akt Signal Transduction Pathways Stat3 protein epithelial to mesenchymal transition
Content Type	Text
Resource Type	Article

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