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Dysregulated Fatty Acid Metabolism in Hepatocellular Carcinoma
( Ming-da Wang ),( Jun Han ),( Hao Xing ),( Han Zhang ),( Zheng Wang ),( Zhen-li Li ),( Liang Lei ),( Chao Li ),( Feng Shen ),( Tian Yang ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Studies are urgently needed on it molecular pathogenesis and biological characteristics of hepatocellular carcinoma (HCC). Dysregulation of fatty acid (FA) metabolism, in which aberrant activation of oncogenic signaling pathways alters the expression and activity of lipid-metabolizing enzymes, is an emerging hallmark of cancer cells, and it may be involved in HCC development and progression. Methods: We summarize the characteristics of FA metabolism in HCC, focusing on the pathways of FA synthesis, oxidation, uptake and transport. We also provide a brief review of the relationship between NAFLD and HCC development. Results: The current review summarizes the dysregulated FA metabolism in HCC and pathways through which this dysregulation may regulate HCC survival and growth. Aberrant activation of oncogenic signaling pathways regulates the expression and activity of lipid-metabolizing enzymes, thus reprogramming FA metabolism to promote HCC development and progression. Intracellular FAs are required for biosynthesis of most biological membrane lipids and signaling molecules, and are also used to provide energy to support HCCs survival and proliferation, when necessary, through β-oxidation process. HCC cells can employ appropriate metabolic pathways as different situation demands. Intrahepatic cholangiocarcinoma (ICC) and HCC exhibits differential requirement for de novo lipogenesis and distinct response to therapeutic approaches focusing on inhibition of exogenous FA uptake. Non-alcoholic fatty liver disease related obesity and diabetes have increasingly emerged as two major factors responsible for the rise in prevalent of HCC. Conclusions: Our understanding of dysregulated FA metabolism and associated signaling pathways may contribute to the development of novel and efficient anti-tumor approaches for patients with HCC.
Reduced Telomere Length in Colorectal Carcinomas
Feng, Tong-Bao,Cai, Lei-Ming,Qian, Ke-Qing,Qi, Chun-Jian Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.2
Purpose: Telomeres play a key role in the maintenance of chromosome integrity and stability, and telomere shortening is involved in initiation and progression of malignancies. The aim of this study was to determine whether telomere length is associated with the colorectal carcinoma. Patients and methods: A total of 148 colorectal cancer (CRC) samples and corresponding adjacent non-cancerous tissues were evaluated for telomere length, P53 mutation, and cyclooxygenase-2 (COX-2) mutation detected by fluorescent immunohistochemistry. Telomere length was estimated by real-time PCR. Samples with a T/S>1.0 have an average telomere length greater than that of the standard DNA; samples with a T/S<1.0 have an average telomere length shorter than that of the standard DNA. Results: Telomeres were shorter in CRCs than in adjacent tissues, regardless of tumor stage and grade, site, or genetic alterations (P=0.004). Telomere length in CRCs also had differences with COX-2 status (P=0.004), but did not differ with P53 status (P=0.101), tumor progression (P=0.244), gender (P=0.542), and metastasis (P=0.488). There was no clear trend between T/S optimal cut-off values (<1 or > 1) and colorectal tumor progression, metastasis, gender, P53 and COX-2 status. Conclusion: These findings suggesting that telomere shortening is associated with colorectal carcinogenesis but does not differ with tumor progression, gender, and metastasis.