Association of GSTP1 and P16 promoter methylation with the risk of HBV-related hepatocellular carcinoma: a meta-analysis

Li, Qin; Deng, Chuiwen; Zhang, Ting; Li, Xiang

doi:10.2147/ott.s168444

Cited by 3 publications

(2 citation statements)

References 38 publications

(34 reference statements)

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“…However, recent research shows that GSTP1 is closely related to tumor occurrence and prognosis [60][61][62][63]. GSTP1 is highly expressed in a variety of tumor tissues and can be used as a biomarker in tumors [64][65][66]. Therefore, research needs to further explore the role of GSTP1 in tumor tissue after radiotherapy, so that clinic can make individual treatment for patients to reduce the occurrence of RILI.…”

Section: Perspectivementioning

confidence: 99%

GSTP1 as a novel target in radiation induced lung injury

Xiao

Wang

et al. 2021

J Transl Med

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The glutathione S-transferase P1(GSTP1) is an isoenzyme in the glutathione-S transferases (GSTs) enzyme system, which is the most abundant GSTs expressed in adult lungs. Recent research shows that GSTP1 is closely related to the regulation of cell oxidative stress, inhibition of cell apoptosis and promotion of cytotoxic metabolism. Interestingly, there is evidence that GSTP1 single nucleotide polymorphisms (SNP) 105Ile/Val related to the risk of radiation induced lung injury (RILI) development, which strongly suggests that GSTP1 is closely associated with the occurrence and development of RILI. In this review, we discuss our understanding of the role of GSTP1 in RILI and its possible mechanism.

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Section: Perspectivementioning

confidence: 99%

GSTP1 as a novel target in radiation induced lung injury

Xiao

Wang

et al. 2021

J Transl Med

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“…Furthermore, in 60–85% of human HCC specimens, the p16 INK4A gene is inactivated by the GpG methylation of its promoter [125]. A recent meta-analysis showed a strong association between GSTP1 (glutathione s-transferase, PI) and P16 INK4A gene promoter methylation and an increase in HBV-related HCC susceptibility [126].…”

Section: Human Hepatocarcinogenesismentioning

confidence: 99%

Experimental Models to Define the Genetic Predisposition to Liver Cancer

Pascale

Simile

Peitta

et al. 2019

Cancers

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Hepatocellular carcinoma (HCC) is a frequent human cancer and the most frequent liver tumor. The study of genetic mechanisms of the inherited predisposition to HCC, implicating gene–gene and gene–environment interaction, led to the discovery of multiple gene loci regulating the growth and multiplicity of liver preneoplastic and neoplastic lesions, thus uncovering the action of multiple genes and epistatic interactions in the regulation of the individual susceptibility to HCC. The comparative evaluation of the molecular pathways involved in HCC development in mouse and rat strains differently predisposed to HCC indicates that the genes responsible for HCC susceptibility control the amplification and/or overexpression of c-Myc, the expression of cell cycle regulatory genes, and the activity of Ras/Erk, AKT/mTOR, and of the pro-apoptotic Rassf1A/Nore1A and Dab2IP/Ask1 pathways, the methionine cycle, and DNA repair pathways in mice and rats. Comparative functional genetic studies, in rats and mice differently susceptible to HCC, showed that preneoplastic and neoplastic lesions of resistant mouse and rat strains cluster with human HCC with better prognosis, while the lesions of susceptible mouse and rats cluster with HCC with poorer prognosis, confirming the validity of the studies on the influence of the genetic predisposition to hepatocarinogenesis on HCC prognosis in mouse and rat models. Recently, the hydrodynamic gene transfection in mice provided new opportunities for the recognition of genes implicated in the molecular mechanisms involved in HCC pathogenesis and prognosis. This method appears to be highly promising to further study the genetic background of the predisposition to this cancer.

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Contribution of polyol pathway, p16, and tristetraprolin to chemically induced liver injury

Refaat

Maria

Keshk

et al. 2021

Tanta Medical Journal

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Background Hepatocellular carcinoma (HCC) is the most common cause of mortality and morbidity related to cancer in Egypt. Garlic with its organosulfur content has the ability to lower the risk of certain cancers. Aims The aim was to see the importance of polyol pathway, redox status, p16, and RNA-binding protein tristetraprolin (TTP) in chemically induced liver injury and subsequent cancer in addition to the role played by garlic extract in chemoprevention. Materials and methods In total, 50 male rats were allocated in four groups at random. Group II received garlic extract (0.4 g/100 g body weight) by oral gavage, HCC was induced chemically in groups III and IV by single intraperitoneal dose of diethylnitrosamine (200 mg/kg body weight) and maintained on a weekly subcutaneous injection of carbon tetrachloride (3 ml/kg body weight) for 10 weeks. Group IV received garlic extract in parallel with the induction. Hepatic p16 and TTP levels were immunoassayed. Moreover, hepatic function tests, aldose reductase activity, and redox status (malondialdehyde and catalase) were evaluated, in addition to the histological evaluation. Results Aspartate aminotransferase, alanine aminotransferase, hepatic malondialdehyde level, and aldose reductase activity were increased in the HCC group upon induction. Meanwhile, serum albumin, hepatic p16 and TTP level, and catalase activity were decreased. Garlic administration in parallel with the induction reverses the obtained biochemical changes and protected against chemical induction of HCC. Histological findings confirmed the laboratory results. Conclusion Garlic could protect against diethylnitrosamine/carbon tetrachloride −induced HCC and so it may be effective in protecting the liver against chemically induced hepatocyte damage and cancer.

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Association of GSTP1 and P16 promoter methylation with the risk of HBV-related hepatocellular carcinoma: a meta-analysis

Cited by 3 publications

References 38 publications

GSTP1 as a novel target in radiation induced lung injury

GSTP1 as a novel target in radiation induced lung injury

Experimental Models to Define the Genetic Predisposition to Liver Cancer

Contribution of polyol pathway, p16, and tristetraprolin to chemically induced liver injury

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