Long interspersed nuclear element ORF-1 protein promotes proliferation and resistance to chemotherapy in hepatocellular carcinoma

Feng, Fan; Lu, Yinying; Zhang, Fan; Gao, Xudong; Zhang, Chuanfu; Meredith, Alex; Xu, Zhongxian; Yang, Yutao; Chang, Xiujuan; Wang, Hong; Qu, Jing; Zeng, Zhen; Yang, Jing; Wang, Chunping; Zhu, Yaping; Cui, Jiahuan; Yang, Yongping

doi:10.3748/wjg.v19.i7.1068

Cited by 30 publications

(23 citation statements)

References 17 publications

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“…Subsequently, cells were seeded into 96-well plates (8000 cells per well). Following the full attachment of cells to the bottom of the plates, the cells were treated with the indicated concentrations of molecular targeted agents (i.e., 10, 3, 1, 0.3, 0.1, 0.03, and 0.01 μmol/l) for 48 h. Subsequently, the cells were analyzed through Thiazolyl Blue Tetrazolium Bromide [3-(4,5-dimethyl-2thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide] (MTT) analysis following previously described methods 42 . The inhibition rate was calculated as follows: (optical density [OD] 490 nm control group − OD 490 nm administration group)/(OD 490 nm control group) 43,44 .…”

Section: Examination Of Cell Survival Using the Mtt Methodsmentioning

confidence: 99%

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

et al. 2019

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Molecular targeted agents, such as sorafenib, remain the only choice of an antitumor drug for the treatment of advanced hepatocellular carcinoma (HCC). The Notch signaling pathway plays central roles in regulating the cellular injury/stress response, anti-apoptosis, or epithelial-mesenchymal transition process in HCC cells, and is a promising target for enhancing the sensitivity of HCC cells to antitumor agents. The ADAM metalloprotease domain-17 (ADAM-17) mediates the cleavage and activation of Notch protein. In the present study, microRNA-3163 (miR-3163), which binds to the 3′-untranslated region of ADAM-17, was screened using online methods. miRDB and pre-miR-3163 sequences were prepared into lentivirus particles to infect HCC cells. miR-3163 targeted ADAM-17 and inhibited the activation of the Notch signaling pathway. Infection of HCC cells with miR-3163 enhanced their sensitivity to molecular targeted agents, such as sorafenib. Therefore, miR-3163 may contribute to the development of more effective strategies for the treatment of advanced HCC.

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Section: Examination Of Cell Survival Using the Mtt Methodsmentioning

confidence: 99%

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

et al. 2019

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“…L-02 (a nontumor hepatic cell line) HCC cell lines, HepG2 (an HCC cells line), LM-3 (a highly aggressive HCC cell line), MHCC97-H cells (a highly aggressive HCC cell line), Hu7 (an HCC cell line), BEL-7402 (an HCC cell line), MHCC97-L (a lowly aggressive HCC cell line), and SMMC-7721 (an HCC cell line), which were purchased from the Type Culture Collection of the Chinese Academy of Sciences (Shanghai, People's Republic of China) or the National Infrastructure of Cell Line Resources, Chinese Academy of Medical Sciences (Beijing, People's Republic of China), the culture collection centers of the Chinese government, have been described in our previous publication and were maintained under conditions described in our previous work. [31][32][33][34] ARQ-197 (catalog no. S2753) or sorafenib (catalog no.…”

Section: Materials and Methods Cell Line And Reagentsmentioning

confidence: 99%

<p>ARQ-197 enhances the antitumor effect of sorafenib in hepatocellular carcinoma cells via decelerating its intracellular clearance</p>

Gao¹,

Chen²,

Huang³

et al. 2019

OTT

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Background: Hepatocellular carcinoma (HCC) is one of the heaviest malignant burdens in China. Molecular targeting agent, sorafenib, is the main therapeutic option for antitumor therapy of advanced HCC, but it is currently too expensive for the public and its therapeutic effect does not satisfy initial expectation. Therefore, it is important to develop more effective molecular targeted therapeutic strategies for advanced HCC. Materials and methods: The antitumor effects of sorafenib or ARQ-197, an antagonist of c-MET (tyrosine-protein kinase Met or hepatocyte growth factor receptor), were examined by MTT or in murine tumor model. The effect of ARQ-197 on epithelial-mesenchymal transition (EMT) or multidrug resistance (MDR) was examined by quantitative real-time PCR for the expression of related genes. The clearance of sorafenib in HCC cells was detected by liquid chromatography-mass spectrometry/mass spectrometry. Results: ARQ-197 treatment enhanced the sensitivity of HCC cells to sorafenib. Mechanistic studies indicated that ARQ-197 inhibited the expression of EMT-and MDR-related genes. Moreover, ARQ-197 treatment decelerated the clearance of sorafenib in cultured HCC cells and subcutaneous HCC tumors in nude mice. Conclusion: In the present work, our data suggested that ARQ-197 decelerated the clearance of sorafenib in HCC cells and enhanced the antitumor effect of sorafenib.

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“…Sorafenib concentrations were selected as: 10, 3, 1, 0.3, 0.1, 0.03, or 0.01 μmol/L. The inhibition rates of sorafenib on HCC cells were calculated as (OD 490 control group − OD 490 administration group)/(OD 490 control group − OD 490 blank group) × 100% 15,16…”

Section: Methodsmentioning

confidence: 99%

Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

Chen

Jiang

Zhang

2018

CMAR

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BackgroundThe application of the oral targeted therapeutic agent sorafenib provides new hope for patients suffering from advanced stages of hepatocellular carcinoma (HCC), but the prognosis of such patients remains poor due to the rapid development of the multidrug resistance process in cancer pathogenesis. The present work evaluated whether copine-III, a novel cancer regulator encoded by the CPNE3 gene, would be a potential indicator of sorafenib resistance in HCC treatment.Materials and methodsThe endogenous expression of copine-III in clinical specimens was examined by quantitative polymerase chain reaction. Copine-III siRNA was transfected into HCC cells to downregulate copine-III expression. The effect of copine-III on sorafenib’s antitumor activation was identified by in vitro and in vivo experiments (MTT, Transwell, and flow cytometry as well as a nude mice model).ResultsHigh levels of copine-III in clinical specimens are related to poor prognosis of advanced HCC patients on sorafenib treatment. Infection of Ad-siCPNE3 significantly decreased the endogenous expression of copine-III and enhanced the susceptibility of MHCC97-H cells to sorafenib: the IC50 value decreased from 1.15±0.11 to 0.25±0.05 μmol/L. Moreover, silencing copine-III enhanced the effect of sorafenib on apoptosis, in vitro invasion/migration, and subcutaneous or intrahepatic growth of MHCC97-H cells in nude mice.ConclusionCopine-III is a novel potential indicator of prognosis for patients who received sorafenib for advanced HCC treatment.

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Long interspersed nuclear element ORF-1 protein promotes proliferation and resistance to chemotherapy in hepatocellular carcinoma

Cited by 30 publications

References 17 publications

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

<p>ARQ-197 enhances the antitumor effect of sorafenib in hepatocellular carcinoma cells via decelerating its intracellular clearance</p>

Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

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