Hepatocellular Carcinoma

El–Serag, Hashem B.

doi:10.1056/nejmra1001683

Cited by 3,358 publications

(2,871 citation statements)

References 53 publications

(36 reference statements)

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“…Hepatocellular carcinoma (HCC), a chronic inflammation‐related cancer, is the second highest cause of cancer death globally as a result of tumor metastasis and early post‐surgery recurrence (El‐Serag, 2011; Galun, 2016; Villanueva and Llovet, 2014). Despite recent studies identifying many cancer‐related factors in HCC metastasis, the underlying mechanism of HCC progression remains largely unknown (Forner et al ., 2012).…”

Section: Introductionmentioning

confidence: 99%

Retracted:HBx‐mediated decrease of AIM2 contributes to hepatocellular carcinoma metastasis

Chen

Liu

et al. 2017

Molecular Oncology

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Tumor metastasis is responsible for the high mortality rates in patients with hepatocellular carcinoma (HCC). Absent in melanoma 2 (AIM2) has been implicated in inflammation and carcinogenesis, although its role in HCC metastasis remains unknown. In the present study, we show that AIM2 protein expression was noticeably reduced in HCC cell lines and clinical samples. A reduction in AIM2 was closely associated with higher serum AFP levels, vascular invasion, poor tumor differentiation, an incomplete tumor capsule and unfavorable postsurgical survival odds. In vitro studies demonstrated that AIM2 expression was modulated by hepatitis B virus X protein (HBx) at transcriptional and post‐translational levels. HBx overexpression markedly blocked the expression of AIM2 at mRNA and protein levels by enhancing the stability of Enhancer of zeste homolog 2 (EZH2). Furthermore, HBx interacted with AIM2, resulting in an increase of AIM2 degradation via ubiquitination induction. Functionally, knockdown of AIM2 enhanced cell migration, formation of cell pseudopodium, wound healing and tumor metastasis, whereas reintroduction of AIM2 attenuated these functions. The loss of AIM2 induced the activation of epithelial‐mesenchymal transition (EMT). Fibronectin 1 (FN1) was found to be a downstream effector of AIM2, with its expression reversely modulated by AIM2. Silencing of FN1 significantly halted cell migration induced by AIM2 depletion. These data demonstrate that HBx‐induced loss of AIM2 is associated with poor outcomes and facilitates HCC metastasis by triggering the EMT process. The results of the present study therefore suggest that AIM2 is a potential prognostic biomarker in hepatitis B virus‐related HCC, as well as a possible therapeutic target for tumor metastasis.

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Section: Introductionmentioning

confidence: 99%

Retracted:HBx‐mediated decrease of AIM2 contributes to hepatocellular carcinoma metastasis

Chen

Liu

et al. 2017

Molecular Oncology

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“…Indeed, apart from the histopathological diagnosis of cirrhosis, at least from a clinical point of view, one should not consider cirrhosis as an end point. Rather, it has been suggested the need to define at least two distinct stages of cirrhosis [8] …”

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confidence: 99%

Cellular and molecular mechanisms in liver fibrogenesis

Novo

Cannito

Paternostro

et al. 2014

Archives of Biochemistry and Biophysics

171

192

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“…Hepatocellular carcinoma is the most common type of primary liver cancer and the third leading cause of cancer deaths worldwide (El‐Serag, 2011). In our previous research, we found that the expression of CSIG was increased in HCC tissue and promoted HCC proliferation.…”

Section: Resultsmentioning

confidence: 99%

“…Hepatocellular carcinoma is the most common type of primary liver cancer and the third leading cause of cancer deaths worldwide (El‐Serag, 2011); However, the underlying mechanism of HCC is complex and largely unknown. The effects of many chemotherapeutic drugs targeting rRNA synthesis or maturation have received increasing attention in recent years (Brighenti et al ., 2015).…”

Section: Discussionmentioning

confidence: 99%

Enhanced NOLC1 promotes cell senescence and represses hepatocellular carcinoma cell proliferation by disturbing the organization of nucleolus

Yuan

Zhang

et al. 2017

Aging Cell

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SummaryThe nucleolus is a key organelle that is responsible for the synthesis of rRNA and assembly of ribosomal subunits, which is also the center of metabolic control because of the critical role of ribosomes in protein synthesis. Perturbations of rRNA biogenesis are closely related to cell senescence and tumor progression; however, the underlying molecular mechanisms are not well understood. Here, we report that cellular senescence‐inhibited gene (CSIG) knockdown up‐regulated NOLC1 by stabilizing the 5′UTR of NOLC1 mRNA, and elevated NOLC1 induced the retention of NOG1 in the nucleolus, which is responsible for rRNA processing. Besides, the expression of NOLC1 was negatively correlated with CSIG in the aged mouse tissue and replicative senescent 2BS cells, and the down‐regulation of NOLC1 could rescue CSIG knockdown‐induced 2BS senescence. Additionally, NOLC1 expression was decreased in human hepatocellular carcinoma (HCC) tissue, and the ectopic expression of NOLC1 repressed the proliferation of HCC cells and tumor growth in a HCC xenograft model.

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Hepatocellular Carcinoma

Cited by 3,358 publications

References 53 publications

Retracted:HBx‐mediated decrease of AIM2 contributes to hepatocellular carcinoma metastasis

Retracted:HBx‐mediated decrease of AIM2 contributes to hepatocellular carcinoma metastasis

Cellular and molecular mechanisms in liver fibrogenesis

Enhanced NOLC1 promotes cell senescence and represses hepatocellular carcinoma cell proliferation by disturbing the organization of nucleolus

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