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Abnormally high HIP1 expression is associated with metastatic behaviors and poor prognosis in ESCC.

Abstract
Huntingtin interacting protein 1 (HIP1) is overexpressed in several human malignancies. However, the biological function of HIP1 in esophageal squamous cell carcinoma (ESCC), and its effect on the prognosis of patients remain unclear. The present study aimed to investigate HIP1 expression in ESCC via immunohistochemistry, reverse transcription-quantitative PCR and western blot analyses. The association between HIP1 expression and the clinicopathological characteristics of 173 patients with ESCC was statistically analyzed. The effect of HIP1 expression on patient prognosis was assessed via Kaplan-Meier and Cox regression analyses. Lentivirus-delivered RNA interfering technique was used to overexpress and downregulate HIP1 expression in ESCC cell lines. The results demonstrated that HIP1 expression was significantly higher in ESCC tissues compared with adjacent normal tissues, and HIP1 expression was associated with histological differentiation, tumor-node-metastasis stage and lymph node metastasis. Furthermore, the overall survival time of patients with high HIP1 expression was significantly shorter than those with low HIP1 expression. Cellular mobility demonstrated that overexpressing HIP1 increased ESCC proliferation, migration and invasion, whereas silencing HIP1 decreased ESCC proliferation, migration and invasion. Furthermore, overexpressing HIP1 induced ESCC cells to enter the S and G2 phases from the G1 phase, whereas HIP1 knockdown arrested the cell cycle in the G1 phase. Taken together, the results of the present study suggest that HIP1 is associated with proliferation and metastatic behaviors in ESCC, and thus may be used as a potential prognostic indicator for patients with ESCC.
AuthorsYing Sun, Yongan Zhou, Jinghua Xia, Miaomiao Wen, Xuejiao Wang, Jiao Zhang, Yanning Zhang, Zhipei Zhang, Tao Jiang
JournalOncology letters (Oncol Lett) Vol. 21 Issue 2 Pg. 79 (Feb 2021) ISSN: 1792-1074 [Print] Greece
PMID33363616 (Publication Type: Journal Article)
CopyrightCopyright: © Sun et al.

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