CHD1L is associated with poor survival and promotes the proliferation and metastasis of intrahepatic cholangiocarcinoma Corrigendum in /10.3892/or.2019.7262

Li,Shimiao; Chai,Yi; Ding,Yanbao; Yuan,Tinghao; Wu,Changwen; Huang,Changwen

doi:10.3892/or.2019.7174

CHD1L is associated with poor survival and promotes the proliferation and metastasis of intrahepatic cholangiocarcinoma

Corrigendum in: /10.3892/or.2019.7262

Authors:
- Shimiao Li
- Yi Chai
- Yanbao Ding
- Tinghao Yuan
- Changwen Wu
- Changwen Huang
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Affiliations: Department of Hepatobiliary Surgery, Jiangxi Provincial People's Hospital, Nanchang, Jiangxi 330006, P.R. China, Department of Neurosurgery, Yuquan Hospital, School of Clinical Medicine, Tsinghua University, Beijing 100040, Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Department of Urology Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
Published online on: May 28, 2019 https://doi.org/10.3892/or.2019.7174
Pages: 657-669
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Chromodomain helicase/ATPase DNA‑binding protein 1‑like gene (CHD1L) is a new oncogene which has been confirmed to be crucial to the progression of many solid tumors. In the present study, the expression of CHD1L was found to be upregulated in intrahepatic cholangiocarcinoma (ICC), which was significantly associated with histological differentiation (P=0.011), vascular invasion (P=0.002), lymph node metastasis (P=0.008) and TNM stage (P=0.001). Kaplan‑Meier survival analysis revealed that ICC patients with positive CHD1L expression had shorter overall and disease‑free survival than those with negative CHD1L expression. Functional study found that CHD1L exhibited strong oncogenic roles, including increased cell growth by CCK‑8 assay, colony formation by plate colony formation assay, G1/S transition by ﬂow cytometry and tumor formation in nude mice. In addition, RNAi‑mediated silencing of CHD1L inhibited ICC invasion and metastasis by wound healing, Transwell migration and Matrigel invasion assays in vitro and in vivo. Collectively, our results show that CHD1L is upregulated and promotes the proliferation and metastasis of ICC cells. CHD1L acts as an oncogene and may be a prognostic factor or therapeutic target for patients with ICC.

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