Fatty changes associated with N-Nitrosodiethylamine (DEN) induced hepatocellular carcinoma: a role of sonic hedgehog signaling pathway.

Q2 Biochemistry, Genetics and Molecular Biology
Anindita Tripathy, Sudhir Thakurela, Manoj Kumar Sahu, Kanishka Uthansingh, Ayaskanta Singh, Jimmy Narayan, Amrendra Kumar Ajay, Vinay Singh, Ratna Kumari
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引用次数: 7

Abstract

Backgrounds and aims: Hepatocellular Carcinoma (HCC) is the leading cause of cancer-related mortality across the world. Non-viral etiological factors including obesity and metabolic syndrome have now become prevalent cause of hepatocellular carcinoma. Sonic Hedgehog (SHH) pathway is activated in hepatocellular carcinoma but its role in regulation of lipogenic molecules during the hepatocarcinogenesis is not known. The aim of present study is to explore the role of SHH pathway in fatty changes associated with hepatocarcinogenesis at different stages and to further correlate the expression of SHH with lipogenic pathways.

Results: Our results demonstrated significant increase in lipidosis and fibrosis in DEN+CCl4 treated animals. It was simultaneously associated with the enhanced expression level of SHH, E2F1, adiponectin, and lipogenic molecules in DEN+CCl4 treated animals. These results were also corroborated with the similar findings in higher stage patients' biospecimens.

Methods: N-Nitrosodiethylamine (DEN) and Carbon TetraChloride (CCl4) induced hepatocellular acrcinoma model in male Wistar rats were established to study the expression level of SHH pathway and associated fatty changes during different stages of hepatocarcinogenesis. The expression levels of SHH, E2F1, and lipogenic molecules were checked at different stages of hepatocellular carcinoma. These results were further compared with biospecimens of hepatocellular carcinoma patients of different stages.

Conclusions: Our results revealed an unknown aspect of SHH pathway in hepatocarcinogenesis via its control over lipogenesis. It gives insight into the lipogenic properties of DEN+CCl4 induced rodent hepatocarcinogenesis model and how SHH pathway operate to arbitrate this response.

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与n -亚硝基二乙胺(DEN)诱导的肝细胞癌相关的脂肪变化:sonic hedgehog信号通路的作用
背景和目的:肝细胞癌(HCC)是全球癌症相关死亡的主要原因。非病毒性病因包括肥胖和代谢综合征已成为肝细胞癌的主要病因。Sonic Hedgehog (SHH)通路在肝细胞癌中被激活,但其在肝癌发生过程中调控脂质分子的作用尚不清楚。本研究旨在探讨SHH通路在不同阶段与肝癌发生相关的脂肪变化中的作用,并进一步将SHH的表达与脂肪生成通路联系起来。结果:我们的研究结果显示,DEN+CCl4治疗动物的脂质沉积和纤维化显著增加。在DEN+CCl4处理的动物中,它同时与SHH、E2F1、脂联素和脂肪生成分子的表达水平升高有关。这些结果也与高分期患者生物标本的类似发现相证实。方法:建立n -亚硝基二乙胺(DEN)和四氯化碳(CCl4)诱导的雄性Wistar大鼠肝细胞癌模型,研究肝癌发生不同阶段SHH通路的表达水平及相关脂肪变化。检测肝细胞癌不同分期SHH、E2F1和脂质生成分子的表达水平。这些结果进一步与不同分期肝癌患者的生物标本进行比较。结论:我们的研究结果揭示了SHH通路通过其对脂肪生成的控制在肝癌发生中的未知方面。它揭示了DEN+CCl4诱导的啮齿动物肝癌模型的脂质特性以及SHH通路如何运作以仲裁这种反应。
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来源期刊
Genes and Cancer
Genes and Cancer Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.90
自引率
0.00%
发文量
6
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