Association Between Insulin-like Growth Factor-2 Expression and Prognosis after Transcatheter Arterial Chemoembolization and Octreotide in Patients with Hepatocellar Carcinoma

Xiong, Zeng; Huang, Fang; Lu, Min-qiang

doi:10.7314/apjcp.2012.13.7.3191

Cited by 9 publications

(6 citation statements)

References 14 publications

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“…Soon et al reported that high miR-483-5p expression predicted for poor overall specific survival in adrenocortical carcinomas [ 31 ]; Chabre et al also found that high serum miR-483-5p level was associated with both shorter recurrence-free survival and shorter overall survival in adrenocortical cancer patients [ 32 ]; similarly, Wang et al reported that high serum miR-483-5p concentration was related to poor survival outcome in patients with nasopharyngeal carcinoma [ 47 ]. On the other hand, Dong et al reported that serum IGF-II level was correlated with extrahepatic metastases in HCC patients [ 48 ]; Xion et al observed that the increase of IGF-II level in serum appeared to be associated with the occurrence of metastatic HCC after TACE and chemotherapy [ 49 ]; Sayer et al found that high IGF-II expression was an independent predictor of poor survival in patients with epithelial ovarian cancer [ 50 ]. The above findings indicate that the overexpression of both miR-483-5p and IGF-II may be associated with poor clinical outcome in cancer.…”

Section: Discussionmentioning

confidence: 99%

MiR-483-5p promotes IGF-II transcription and is associated with poor prognosis of hepatocellular carcinoma

et al. 2017

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The human insulin-like growth factor-II (IGF-II) gene transcribes four mRNAs (P1 mRNA-P4 mRNA), and P3 mRNA overexpression contributes to hepatocarcinogenesis. IGF-II-derived miR-483-5p is implicated in the development of cancers. Here, we investigated the involvement of miR-483-5p in P3 mRNA overexpression regulation and its role in hepatocellular carcinoma. Our results showed that miR-483-5p up-regulated P3 mRNA transcription by targeting the 5′-untranslated region (5′UTR) of P3 mRNA in hepatocellular carcinoma. The mechanism was involved in recruiting of an argonaute 1(Ago1)-argonaute 2 (Ago2) complex to the P3 mRNA 5′UTR and the P3 promoter of IGF-II gene by miR-483-5p, accompanied by increased enrichment of RNA polymerase II and activating histone marks histone 3 lysine 4 trimethylation (H3K4me3), histone 3 lysine 27 acetylation (H3K27ac), and histone 4 lysine 5/8/12/16 acetylation (H4Kac) at the P3 promoter. High miR-483-5p expression was an independent predictor for shorter survival of HCC patients. The findings suggest that miR-483-5p promotes P3 mRNA transcription by recruiting the Ago1-Ago2 complex to the P3 mRNA 5′UTR and is associated with poor prognosis of HCC. Our results display a potential new model for miRNAs to up-regulate gene expression.

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Section: Discussionmentioning

confidence: 99%

MiR-483-5p promotes IGF-II transcription and is associated with poor prognosis of hepatocellular carcinoma

et al. 2017

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“…Tumor genetics vary in HCC and multiple genetic markers have been associated with tumor progression and recurrence (15-17). Recent reports further reveal that TACE and RFA affect molecular markers related to tumor aggressiveness and thus MMT may serve to uncover and, in certain cases, alter the underlying tumor biology (18,19). Clinically, patients presenting with higher tumor stage and AFP usually do not progress to transplant due to concerns that they harbor more advanced and biologically active tumors (20).…”

Section: Discussionmentioning

confidence: 99%

Multimodality Therapy and Liver Transplantation for Hepatocellular Carcinoma

et al. 2014

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Background Hepatocellular carcinoma is a major cause of death among patients with cirrhosis. A standardized approach of multimodality therapy with intent-to-treat by transplantation for all patients with hepatocellular carcinoma was instituted at our transplant center in 1997. Data were prospectively collected to evaluate the impact of multimodality therapy on post-transplant patient survival, tumor recurrence and patient survival without transplantation. Methods All patients with hepatocellular carcinoma were eligible for multimodality therapy. Multimodality therapy consisted of hepatic resection, radiofrequency ablation, transarterial chemoembolization, transarterial chemoinfusion, yttrium-90 microsphere radioembolization and sorafenib. Results 715 patients underwent multimodality therapy. 231 patients were included in the intent-to-treat with transplantation arm and 484 patients were treated with multimodality therapy or palliative therapy due to contraindications for transplantation. A 60.2% transplantation rate was achieved in the intent-to-treat with transplantation arm. Post-transplant survivals at 1- and 5-years were 97.1% and 72.5% respectively. Tumor recurrence rates at 1-, 3- and 5-years were 2.4%, 6.2% and 11.6% respectively. Patients with contraindications to transplant had increased 1- and 5-year survival from diagnosis with multimodality therapy compared to those not treated (73.1% and 46.5% vs. 15.5% and 4.4%, p<0.0001). Conclusions Using multimodality therapy prior to liver transplantation for hepatocellular carcinoma achieved low recurrence rates and post-transplant survival equivalent to patients with primary liver disease without hepatocellular carcinoma. Multimodality therapy may help identify patients with less active tumor biology and result in improved disease-free survival and organ utilization.

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“…Finally, it would be interesting in future to see if there are additional differences between viral and alcoholic related HCC like differential expression of receptors or production of trophic factors. In a recent study an increase of serum IGF2 level was reported to be associated with the occurrence of HCC metastasis after TACE and octreotide, as metastatic foci were found in 97% when IGF2 was increasing in contrast to only 13.6% of patients with an IGF2 decrease [141] . In the context of the previous discussion, it should be noted that the expression of IGF2 in HCC was strongly associated with HBV infection [142] .…”

Section: Resultsmentioning

confidence: 94%

Somatostatin in hepatocellular carcinoma: experimental and therapeutic implications

Samonakis¹,

Notas²

2018

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The neuropeptide somatostatin has been shown to control the secretion of several hormones and growth factors, but also to inhibit the proliferation of several tumor cells. Hepatocellular carcinoma (HCC) is a leading cause of death all over the world due to very limited treatment modalities. Early reports showed that somatostatin may influence HCC growth, making somatostatin a potential therapeutic candidate. The introduction of somatostatin analogues with long half-lives has made this prospect feasible. In this review, experimental data regarding the presence of somatostatin receptors and their functional significance in HCC are presented. Potential mechanisms of direct anti-tumoral activity of somatostatin, including effects on tumor cell proliferation and apoptosis, inhibition of various trophic factors and angiogenesis are also reviewed, as well as indirect actions affecting liver fibrosis, inflammation and macrophage-associated innate immunity. Data on the use of somatostatin analogues for the treatment of induced HCC in experimental animals are presented and human studies of somatostatin treatment of advanced HCC are critically analyzed. Reasons and pitfalls for treatment failures are identified and indications for the proper use of somatostatin, either alone or as an adjunct to other modalities in future trials are proposed.

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Association Between Insulin-like Growth Factor-2 Expression and Prognosis after Transcatheter Arterial Chemoembolization and Octreotide in Patients with Hepatocellar Carcinoma

Cited by 9 publications

References 14 publications

MiR-483-5p promotes IGF-II transcription and is associated with poor prognosis of hepatocellular carcinoma

MiR-483-5p promotes IGF-II transcription and is associated with poor prognosis of hepatocellular carcinoma

Multimodality Therapy and Liver Transplantation for Hepatocellular Carcinoma

Somatostatin in hepatocellular carcinoma: experimental and therapeutic implications

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