Downregulation of ROS-FIG inhibits cell proliferation, colony‑formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells Retraction in /10.3892/ijmm.2023.5335

Deng,Gang; Hu,Chenghuan; Zhu,Lei; Huang,Feizhou; Huang,Wei; Xu,Hongbo; Nie,Wanpin

doi:10.3892/ijmm.2014.1823

Downregulation of ROS-FIG inhibits cell proliferation, colony‑formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells

Retraction in: /10.3892/ijmm.2023.5335

Authors:
- Gang Deng
- Chenghuan Hu
- Lei Zhu
- Feizhou Huang
- Wei Huang
- Hongbo Xu
- Wanpin Nie
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Affiliations: Department of Hepatobiliary and Pancreatic Surgery, the Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of Intensive Care Unit, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China
Published online on: June 27, 2014 https://doi.org/10.3892/ijmm.2014.1823
Pages: 661-668
Copyright: © Deng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver cancer with poor responsiveness to existing drug therapies. Therefore, novel treatment strategies against ICC are required to improve survival. The aim of this study was to demonstrate the role of fused-in-glioblastoma-c-ros-oncogene1 (FIG-ROS) fusion gene in ICC. ROS was positively expressed in ICC tissues and HUCCT1 cells. Plasmids expressing ROS- and FIG-specific shRNAs were constructed and transfected into HUCCT1 cells. The results showed that single transfection of ROS- or FIG-specific shRNA inhibited HUCCT1 cell proliferation, colony formation, cell cycle progression, migration and invasion, while inducing apoptosis. Moreover, the co-inhibition of ROS- and FIG-specific shRNA exhibited stronger effects on HUCCT1 cell proliferation, apoptosis, colony formation, cell cycle progression, migration and invasion, when compared to single inhibition of ROS and FIG. Furthermore, findings of this study suggested that the AKT signaling pathway was involved in the ROS-FIG-mediated biological processes of HUCCT1 cells. In summary, the results suggest that FIG-ROS plays an oncogenic role in ICC. Additionally, ROS1-6290 and FIG-363 segments may become effective therapeutic targets for ICC harboring ROS-FIG fusion protein.

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