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J Drug Target. 2018 May 16:1-19. doi: 10.1080/1061186X.2018.1473408. [Epub ahead of print]

Overexpression of HOXC10 promotes glioblastoma cell progression to a poor prognosis via the PI3K/AKT signaling pathway.

Author information

1
a Department of Neurosurgery , Qingdao Minicipal Hospital , No.1 Jjiaozhou Road, Shibei District , Qingdao Shandong 266011 , P.R. China.
2
b Department of Rehabilitation , Qingdao Central Hospital , No.127 Siliunan Road, Shibei District , Qingdao Shandong 266047 , P.R. China.

Abstract

OBJECTIVE:

The HOX gene is expressed in neoplasias occurred in multiple tissues, such as the colon, lung, and breast. However, the effects of the HOX gene on glioblastoma (GBM) remain poorly understood. We examined HOXC10 expression in GBM tissues and cells, analyzed its effect on GBM prognosis, and finally assessed its possible underlying mechanisms in this study.

METHODS:

HOXC10 expression levels and its prognostic effects on GBM tissues were analyzed based on The Cancer Genome Atlas (TCGA) and ONCOMINE database. Overall survival (OS) analysis was performed using the Kaplan-Meier method and log rank test. Then, expression of HOXC10 was detected in four GBM cell lines using quantitative real-time reverse transcription-PCR (qRT-PCR). In addition, small interfering RNA (si-RNA) was utilized in the U87 cell line with the highest HOXC10 expression to facilitate subsequent in vitro cell experiment. Cell proliferation, migration and invasion were assessed using the Cell Counting Kit-8 (CCK-8) and colony formation assay, wound healing, Transwell assay, respectively in GBM U87 cell after HOXC10 knockdown. Key proteins related to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway were measured by western blotting.

RESULTS:

HOXC10 expression was significantly increased in GBM tissues and cell lines, leading a poor OS in GBM patients. Knockdown of HOXC10 could inhibit the GBM U87 cells proliferation, migration and invasion, as well as decreased expression levels of key proteins in PI3K/AKT signaling pathway.

CONCLUSION:

HOXC10 was overexpressed in GBM tissues and cells, and associated with poor prognosis in GBM patients. Moreover, HOXC10 knockdown inhibited U87 cell proliferation, migration and invasion, which were potentially related to PI3K/AKT signaling pathway activation. Our findings revealed that HOXC10 represent a promising biological target for GBM treatment in the future.

KEYWORDS:

HOXC10; PI3K; cell proliferation; glioblastoma; overall survival

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