Increased expression of ErbB‐2 in liver is associated with hepatitis B × antigen and shorter survival in patients with liver cancer

Liu, Jie; Ahiekpor, Angela; Li, Li; Li, Xianxing; Arbuthnot, Patrick; Kew, Michael C.; Feitelson, Mark A.

doi:10.1002/ijc.24580

Cited by 36 publications

(35 citation statements)

References 44 publications

(87 reference statements)

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“…HER-2 amplification has been reported in breast cancer, and a monoclonal antibody trastuzumab, has become an important therapeutic option for patients with HER-2 amplification (44). However, reports on the status of HER-2 in HCC are conflicting (45)(46)(47)(48). By FISH, we showed a high frequency of deletion for TP53.…”

Section: Detection Of Afp Mrnamentioning

confidence: 63%

“…Amplification of HER-2 was observed in 2 patients with higher CTC counts among the 11 patients analyzed. Such amplifications are uncommon in primary tumors of HCC (45,46), whereas some studies show frequent HER-2 overexpression in HCC (47,48). The frequency of HER-2 amplification of CTCs in HCC needs to be investigated with more patients so as to clarify whether it could be a candidate gene for targeted therapy in HCC.…”

Section: Detection Of Afp Mrnamentioning

confidence: 99%

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Isolation of Circulating Tumor Cells in Patients with Hepatocellular Carcinoma Using a Novel Cell Separation Strategy

Cao²,

Chen³

et al. 2011

Clinical Cancer Research

143

139

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Purpose: To establish a sensitive and specific isolation and enumeration system for circulating tumor cells (CTC) in patients with hepatocellular carcinoma (HCC).Experimental Design: HCC cells were bound by biotinylated asialofetuin, a ligand of asialoglycoprotein receptor, and subsequently magnetically labeled by antibiotin antibody-coated magnetic beads, followed by magnetic separation. Isolated HCC cells were identified by immunofluorescence staining using Hep Par 1 antibody. The system was used to detect CTCs in 5 mL blood. Blood samples spiked with Hep3B cells (ranging from 10 to 810 cells) were used to determine recovery and sensitivity. Prevalence of CTCs was examined in samples from HCC patients, healthy volunteers, and patients with benign liver diseases or non-HCC cancers. CTC samples were also analyzed by FISH.Results: The average recovery was 61% or more at each spiking level. No healthy, benign liver disease or non-HCC cancer subjects had CTCs detected. CTCs were identified in 69 of 85 (81%) HCC patients, with an average of 19 AE 24 CTCs per 5 mL. Both the positivity rate and the number of CTCs were significantly correlated with tumor size, portal vein tumor thrombus, differentiation status, and the disease extent as classified by the TNM (tumor-node-metastasis) classification and the Milan criteria. HER-2 gene amplification and TP53 gene deletion were detected in CTCs.Conclusion: Our system provides a new tool allowing for highly sensitive and specific detection and genetic analysis of CTCs in HCC patients. It is likely clinically useful in diagnosis and monitoring of HCC and may have a role in clinical decision making.

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Section: Detection Of Afp Mrnamentioning

confidence: 63%

Section: Detection Of Afp Mrnamentioning

confidence: 99%

Isolation of Circulating Tumor Cells in Patients with Hepatocellular Carcinoma Using a Novel Cell Separation Strategy

Cao²,

Chen³

et al. 2011

Clinical Cancer Research

143

139

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“…important contributing factor to hepatocellular growth (31), and that ErbB2 upregulation was associated with miR-375 regulation (32). The present study aimed to examine the miR-375 level in human liver cancer tissues and cell lines.…”

Section: Mir-375 Is Downregulated In Human Hcc Previous Studies Havementioning

confidence: 96%

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

Jia

Ding

2018

Oncol Lett

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Abstract. microRNAs (miRNA/miRs) are a class of small non-coding RNAs; they serve important biological roles in tumorigenesis through the regulation of oncogene expression, and they may be used for the diagnosis and treatment of human cancer. miR-375 was identified to exhibit abnormal expression levels in a number of types of tumor; however, the biological role of miR-375 in human hepatocellular carcinoma (HCC) remains incompletely characterized. The present study investigated the expression of miR-375 in human HCC tissues and human liver cancer cell lines; results from a reverse transcription quantitative polymerase chain reaction analysis indicated that the expression of miR-375 was significantly decreased in tissues and live cancer cell lines, compared with normal tissues and PHH cells. Additional studies demonstrated that the upregulation of miR-375 inhibited human liver cancer cell growth via regulation of cell apoptosis. It was also revealed that the receptor tyrosine-protein kinase erbB-2 (ErbB2) gene was a direct target gene of miR-375, and that the regulation of ErbB2 was associated with the human liver cancer growth. Therefore, the present study demonstrated that miR-375 was expressed at low levels both in human HCC tissues and cell line, compared with normal tissues and PHH cells, and that the induction of miR-375 expression may regulate human liver cancer cell function through targeting the ErbB2 gene, which may potentially improve the diagnosis and treatment of patients with HCC in the future.

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“…In breast cancer, ErbB2 was found to upregulate b-catenin via inactivation of GSK-3b by the Erk pathway (13). Also, in hepatocellular carcinoma, upregulation of ErbB-2 expression increased the existence of b-catenin (13,27). Further, a study suggested that serum levels of ErbB2 might be associated with liver dysfunction (28).…”

Section: Discussionmentioning

confidence: 99%

Survival and Inflammation Promotion Effect of PTPRO in Fulminant Hepatitis Is Associated with NF-κB Activation

Jiang

Chen

Hou

et al. 2014

The Journal of Immunology

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Previous investigations demonstrated that protein tyrosine phosphatase, receptor type, O (PTPRO) acts as a tumor suppressor in liver cancer; however, little is known about its role in liver inflammation. Thus, we investigated the role of PTPRO in fulminant hepatitis (FH) using a Con A–induced mouse model. Significantly more severe liver damage, but attenuated inflammation, was detected in PTPRO-knockout (KO) mice, and PTPRO deficiency could confer this phenotype to wild-type mice in bone marrow transplantation. Moreover, hepatocytes with PTPRO depletion were more sensitive to TNF-α–induced apoptosis, and secretion of cytokines was significantly decreased in both T and NK/NKT cells and led to marked impairment of NF-κB activation. Intriguingly, wild-type and PTPRO-KO cells responded equally to TNF-α in activation of IKK, but NF-κB activation was clearly decreased in PTPRO-KO cells. PTPRO associated with ErbB2, and loss of PTPRO potentiated activation of the ErbB2/Akt/GSK-3β/β-catenin cascade. Increased β-catenin formed a complex with NF-κB and attenuated its nuclear translocation and activation. Importantly, in humans, PTPRO was much decreased in FH, and this was associated with enhanced β-catenin accumulation but reduced IFN-γ secretion. Taken together, our study identified a novel PTPRO/ErbB2/Akt/GSK-3β/β-catenin/NF-κB axis in FH, which suggests that PTPRO may have therapeutic potential in this liver disease.

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Increased expression of ErbB‐2 in liver is associated with hepatitis B × antigen and shorter survival in patients with liver cancer

Cited by 36 publications

References 44 publications

Isolation of Circulating Tumor Cells in Patients with Hepatocellular Carcinoma Using a Novel Cell Separation Strategy

Isolation of Circulating Tumor Cells in Patients with Hepatocellular Carcinoma Using a Novel Cell Separation Strategy

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

Survival and Inflammation Promotion Effect of PTPRO in Fulminant Hepatitis Is Associated with NF-κB Activation

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