Serum Insulin-Like Growth Factor-1 (IGF-1): a Novel Prognostic Factor for Early Recurrence of Hepatocellular Carcinoma (HCC)

Yifan, Yao; Mao, Weilin; Dong, Minya; Donglei, Yang; Li, Wenpeng; Chen, Yu

doi:10.7754/clin.lab.2016.160732

Cited by 15 publications

(9 citation statements)

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“…Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in clinical practice, which involves abnormal activation of multiple signaling pathways, including gene mutation, chromosome aberration, abnormal secretion of growth factors and epigenetic changes 29–31. Early diagnosis and effective treatment of HCC is still a worldwide medical problem 32,33.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Non-Coding RNA NEAT1 Promoted Hepatocellular Carcinoma Cell Proliferation and Reduced Apoptosis Through the Regulation of Let-7b-IGF-1R Axis</p>

Liu¹,

Shi²,

Yang³

et al. 2019

OTT

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Background and aimLong non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) is abnormally expressed in various human malignancies, including hepatocellular carcinoma (HCC). Let-7b is a miRNA with the effect of a tumor suppressor gene, and its expression level in various tumor tissues is lower than that in normal tissues. Studies have found that IGF-1R can be abnormally activated in the process of hepatocyte deterioration, and the expression level of IGF-1R in HCC is significantly up-regulated. The aim of this study was to investigate the functional mechanism of NEAT1/let-7b-IGF-1R axis in HCC.MethodsThe expressions of NEAT1 and microRNA (miR)-let-7b in HCC tissues and cell lines were quantified by quantitative real-time PCR (qRT-PCR). The effect of NEAT1 on tumor growth was observed in a mice model of transplanted hepatoma. The effects of down-regulation or up-regulation of NEAT1 expression in HCC cell lines were analysed from the perspectives of cell viability and apoptosis. The binding sites of NEAT1 and miR-let-7b were predicted by biological software. The expression of the miR-let-7b target molecules IGF-1R was detected by Western blotting.ResultsThe results showed that the expressions of NEAT1 were significantly increased, while the expressions of miR-let-7b were decreased in the HCC tissues and cell lines. Additionally, it was found that the expressions of NEAT1 and miR-let-7b showed a negative correlation in HCC tissues. The mouse model experiments confirmed that the interference with NEAT1 expression inhibited the tumor growth. Meanwhile, the cell viability of HepG2/Huh7 cell lines was significantly decreased via the downregulation of NEAT1, whereas the corresponding rates of apoptosis were significantly increased. It was further proven that there was a certain negative regulatory mechanism between NEAT1 and miR-1et-7b, which was related to the expression of IGF-1R.ConclusionThe over-expression of NEAT1 could promote the proliferation of HCC cells by inhibiting the expression of the miR-let-7b regulated by IGF-1R.

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Section: Discussionmentioning

confidence: 99%

<p>Long Non-Coding RNA NEAT1 Promoted Hepatocellular Carcinoma Cell Proliferation and Reduced Apoptosis Through the Regulation of Let-7b-IGF-1R Axis</p>

Liu¹,

Shi²,

Yang³

et al. 2019

OTT

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“…Furthermore, TIA-1 can regulate IGF binding protein-3 (IGFBP3) at the post-transcriptional level in human HCC cells (70). IGFBP3 is the primary binding protein of IGF-I, and IGF-I has been reported to be involved in early HCC relapse (71). Therefore, TIA1-mediated IGFBP3 regulation may serve an important role in HCC relapse.…”

Section: Discussionmentioning

confidence: 99%

In silico identification of EP400 and TIA1 as critical transcription factors involved in human hepatocellular carcinoma relapse

Hong

Fan

et al. 2019

Oncol Lett

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-associated mortality worldwide. Transcription factors (TFs) are crucial proteins that regulate gene expression during cancer progression; however, the roles of TFs in HCC relapse remain unclear. To identify the TFs that drive HCC relapse, the present study constructed co-expression network and identified the Tan module the most relevant to HCC relapse. Numerous hub TFs (highly connected) were subsequently obtained from the Tan module according to the intra-module connectivity and the protein-protein interaction network connectivity. Next, E1A-binding protein p400 (EP400) and TIA1 cytotoxic granule associated RNA binding protein (TIA1) were identified as hub TFs differentially connected between the relapsed and non-relapsed subnetworks. In addition, zinc finger protein 143 (ZNF143) and Yin Yang 1 (YY1) were also identified by using the plugin iRegulon in Cytoscape as master upstream regulatory elements, which could potentially regulate expression of the genes and TFs of the Tan module, respectively. The Kaplan-Meier (KM) curves obtained from KMplot and Gene Expression Profiling Interactive Analysis tools confirmed that the high expression of EP400 and TIA1 were significantly associated with shorter relapse-free survival and disease-free survival of patients with HCC. Furthermore, the KM curves from the UALCAN database demonstrated that high EP400 expression significantly reduced the overall survival of patients with HCC. EP400 and TIA1 may therefore serve as potential prognostic and therapeutic biomarkers.

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“…Longitudinal observation of HCC cases (median follow-up period of 41.8 months) proved that IGF1 level was an independent predictor of poorer survival [ 151 ]. Also, in patients undergoing liver resection for HCC, preoperative low and delayed recovery of IGF1 levels at 30 days after surgery were independent risk factors for early recurrence of this cancer [ 153 ].…”

Section: Evidence From Epidemiologic and Clinicopathological Studimentioning

confidence: 99%

Insulin-Like Growth Factor (IGF) System in Liver Diseases

Adamek

Kasprzak

2018

IJMS

216

149

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Hepatocyte differentiation, proliferation, and apoptosis are affected by growth factors produced in liver. Insulin-like growth factor 1 and 2 (IGF1 and IGF2) act in response to growth hormone (GH). Other IGF family components include at least six binding proteins (IGFBP1 to 6), manifested by both IGFs develop due to interaction through the type 1 receptor (IGF1R). The data based on animal models and/or in vitro studies suggest the role of IGF system components in cellular aspects of hepatocarcinogenesis (cell cycle progression, uncontrolled proliferation, cell survival, migration, inhibition of apoptosis, protein synthesis and cell growth), and show that systemic IGF1 administration can reduce fibrosis and ameliorate general liver function. In epidemiologic and clinicopathological studies on chronic liver disease (CLD), lowered serum levels, decreased tissue expression of IGF1, elevated production of IGF1R and variable IGF2 expression has been noted, from the start of preneoplastic alterations up to the developed hepatocellular carcinoma (HCC) stage. These changes result in well-known clinical symptoms of IGF1 deficiency. This review summarized the current data of the complex role of IGF system components in the most common CLD (nonalcoholic fatty liver disease, cirrhosis, and hepatocellular carcinoma). Better recognition and understanding of this system can contribute to discovery of new and improved versions of current preventive and therapeutic actions in CLD.

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Serum Insulin-Like Growth Factor-1 (IGF-1): a Novel Prognostic Factor for Early Recurrence of Hepatocellular Carcinoma (HCC)

Cited by 15 publications

References 0 publications

<p>Long Non-Coding RNA NEAT1 Promoted Hepatocellular Carcinoma Cell Proliferation and Reduced Apoptosis Through the Regulation of Let-7b-IGF-1R Axis</p>

<p>Long Non-Coding RNA NEAT1 Promoted Hepatocellular Carcinoma Cell Proliferation and Reduced Apoptosis Through the Regulation of Let-7b-IGF-1R Axis</p>

In silico identification of EP400 and TIA1 as critical transcription factors involved in human hepatocellular carcinoma relapse

Insulin-Like Growth Factor (IGF) System in Liver Diseases

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