Article
Endocrinology & Metabolism
Brecht Attema, Aafke W. F. Janssen, Deborah Rijkers, Evert M. van Schothorst, Guido J. E. J. Hooiveld, Sander Kersten
Summary: The study found that long-term low-dose exposure to PFOA and GenX disrupts hepatic lipid metabolism in mice, particularly having adverse effects on the liver. The effects of PFOA and GenX differ in pathways, with PFOA being regulated by multiple nuclear receptors and GenX being entirely mediated by PPARa.
MOLECULAR METABOLISM
(2022)
Article
Gastroenterology & Hepatology
Siying Wang, Yangyang Zhou, Ruobing Yu, Jing Ling, Botai Li, Chen Yang, Zhuoan Cheng, Ruolan Qian, Zhang Lin, Chengtao Yu, Jiaojiao Zheng, Xingling Zheng, Qi Jia, Wei Wu, Qiangxin Wu, Mengnuo Chen, Shengxian Yuan, Wei Dong, Yaoping Shi, Robin Jansen, Chen Yang, Yujun Hao, Ming Yao, Wenxin Qin, Haojie Jin
Summary: The molecular mechanisms underlying hepatocellular carcinoma (HCC) are poorly understood. This study revealed that FTCD is significantly downregulated in HCC and low FTCD levels are associated with worse prognosis and higher risk of HCC development. Loss of FTCD promotes chronic HCC and affects fatty acid and cholesterol metabolism in hepatocytes.
Article
Gastroenterology & Hepatology
Pedro M. Rodrigues, Marta B. Afonso, Andre L. Simao, Tawhidul Islam, Maria M. Gaspar, Colm J. O'Rourke, Monika Lewinska, Jesper B. Andersen, Enara Arretxe, Cristina Alonso, Alvaro Santos-Laso, Laura Izquierdo-Sanchez, Raul Jimenez-Aguero, Emma Eizaguirre, Luis Bujanda, Maria J. Pareja, Carina Prip-Buus, Jesus M. Banales, Cecilia M. P. Rodrigues, Rui E. Castro
Summary: This study evaluated the role of hsa-miRNA-21-5p in the development of hepatocellular carcinoma (HCC) in non-alcoholic fatty liver disease (NAFLD) patients. The expression of hsa-miRNA-21-5p was found to increase with NAFLD severity and was associated with hepatic lipotoxicity. Inhibition of hsa-miRNA-21-5p was shown to prevent the progression of NAFLD to NASH and HCC.
LIVER INTERNATIONAL
(2023)
Article
Biochemistry & Molecular Biology
Magdalene K. Montgomery, Amanuiel Z. Taddese, Jacqueline Bayliss, Shuai Nie, Nicholas A. Williamson, Matthew J. Watt
Summary: Hepatic HexA expression is influenced by lipid availability and steatosis, with overexpression leading to increased hepatic GM3 content and upregulation of enzymes involved in glycated sphingolipid degradation, ultimately resulting in sphingomyelin accumulation in the liver. Additionally, overexpression of HEXA in the liver causes significant changes in cell surface lipid rafts, affecting VLDL processing and secretion, leading to hypertriglyceridemia and ectopic lipid accumulation in peripheral tissues. This study highlights the important role of HEXA in modulating hepatic sphingolipid and lipoprotein metabolism.
Article
Multidisciplinary Sciences
Dan Luo, Bin Jin, Xiangyu Zhai, Jing Li, Chuanyong Liu, Wei Guo, Jingxin Li
Summary: Recent studies have shown that oxytocin plays a crucial role in promoting liver regeneration, with a decline in oxytocin receptors in hepatocytes with age, as well as a decrease in serum oxytocin levels as individuals age. Oxytocin appears to promote liver cell regeneration more effectively in aged mice, potentially through the promotion of autophagy.
Article
Oncology
Andrea Reszegi, Katalin Karaszi, Gabor Toth, Kristof Rada, Lorand Vancza, Lilla Turiak, Zsuzsa Schaff, Andras Kiss, Laszlo Szilak, Gabor Szabo, Gabor Petovari, Anna Sebestyen, Katalin Dezso, Eszter Regos, Peter Tatrai, Kornelia Baghy, Ilona Kovalszky
Summary: Syndecan-1 plays a dual role in tumor development, either promoting or inhibiting tumors depending on the cancer type. In the context of liver cancer, transgenic expression of human syndecan-1 delayed tumor formation by downregulating lipid metabolism, inhibiting mTOR and beta-catenin pathways, and activating Foxo1 and p53 transcription factors. This oncoprotective effect was mediated by a beneficial modulation of lipid metabolism and molecular signaling pathways involved in cell cycle regulation and intermediary metabolism.
Article
Immunology
Haidong Wei, Luming Zhen, Shiquan Wang, Liufei Yang, Shuyue Zhang, Yuanyuan Zhang, Pengyu Jia, Tianyue Wang, Kui Wang, Yan Zhang, Lei Ma, Jianrui Lv, Pengbo Zhang
Summary: The study suggests that treatment with GTA can enhance lipid synthesis and IL-33 expression after ischemic stroke, thus improving blood-brain barrier repair and functional recovery.
JOURNAL OF NEUROINFLAMMATION
(2023)
Article
Oncology
Marta Correia de Sousa, Nicolas Calo, Cyril Sobolewski, Monika Gjorgjieva, Sophie Clement, Christine Maeder, Dobrochna Dolicka, Margot Fournier, Laurent Vinet, Xavier Montet, Jean-Francois Dufour, Bostjan Humar, Francesco Negro, Christine Sempoux, Michelangelo Foti
Summary: Despite being considered a potent oncomiR in human cancers, genetic deletion of miR-21 in mouse models surprisingly promotes hepatocellular carcinoma (HCC) development by affecting various signaling pathways and immune responses. These results challenge the current belief in miR-21 as an oncogene and raise caution regarding using miR-21 inhibition as a therapeutic approach for HCC.
Article
Medicine, Research & Experimental
Shan Huang, Andreas Blutke, Annette Feuchtinger, Uwe Klemm, Robby Zachariah Tom, Susanna M. Hofmann, Andre C. Stiel, Vasilis Ntziachristos
Summary: The study found that multispectral optoacoustic tomography (MSOT) can non-invasively visualize lipids in laboratory mice, particularly for the assessment and monitoring of fatty liver disease. By monitoring the clearance kinetics of indocyanine green in the liver, MSOT can also serve as a biomarker for evaluating the severity of hepatic steatosis.
EMBO MOLECULAR MEDICINE
(2021)
Article
Cell Biology
Haiyan Yang, Qiang Wang, Yuemei Xi, De Xie, Hiroko Morisaki, Takayuki Morisaki, Jidong Cheng
Summary: This study identified a mechanistic link between AMPD2 and hepatic glucose and lipid metabolism. AMPD2-deficient mice exhibited reduced body weight, fat accumulation, and blood glucose levels, while showing increased insulin sensitivity. AMPD2 deficiency also led to altered expression of genes related to fatty acid and cholesterol metabolism.
MOLECULAR AND CELLULAR ENDOCRINOLOGY
(2023)
Article
Immunology
Zhen Tian, Xinyue Wang, Tianshu Han, Changhao Sun
Summary: This study demonstrates that the selective MAO-B inhibitor, selegiline, can reduce body weight gain, hepatic steatosis, and dyslipidemia induced by a high-fat diet. These protective effects may be attributed to improved inflammatory response, oxidative stress, and hepatic lipid metabolism.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Zhenbang Qin, Ping Wang, Weiwen Chen, Jue-Rui Wang, Xianhua Ma, Hai Zhang, Weiping J. Zhang, Chunchun Wei
Summary: This study reveals that hepatic ELOVL3 is not essential for lipid metabolism and does not play a significant role in maintaining lipid homeostasis or the development of obesity and hepatic steatosis. Liver-specific knockout of Elovl3 does not result in abnormalities in body weight, liver mass and morphology, liver triglyceride content, or glucose tolerance under normal or low-fat diet conditions. Moreover, the deletion of hepatic Elovl3 does not significantly affect body weight gain or hepatic steatosis induced by high-fat diet. Lipidomic analysis shows that the loss of hepatic Elovl3 does not cause substantial changes in lipid profiles. Unlike global knockouts, mice lacking Elovl3 specifically in the liver exhibit normal expression of genes involved in hepatic de novo lipogenesis, lipid uptake, or beta-oxidation at the mRNA and protein levels. Overall, our data indicate that hepatic ELOVL3 is dispensable for metabolic homeostasis or diet-induced metabolic disease.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2023)
Article
Endocrinology & Metabolism
Fei Teng, Jingjing Jiang, Jinhua Zhang, Youwen Yuan, Kangli Li, Bing Zhou, Xuan Zhou, Wenhui Liu, Peizhen Zhang, Deying Liu, Minghua Zheng, Yan Lu, Huijie Zhang
Summary: The study demonstrated that S100A11 is upregulated in NAFLD patients and overexpression of S100A11 significantly increases liver steatosis, body weight, and AST levels. Mechanistically, S100A11 acts as a positive regulator of the AKT/mTOR signaling pathway to induce lipid synthesis and aggravate lipid deposition. Targeting S100A11 may be a potential therapeutic approach for NAFLD.
METABOLISM-CLINICAL AND EXPERIMENTAL
(2021)
Article
Chemistry, Medicinal
Jiena Ye, Xiaoxiao Tian, Qiongfen Wang, Jiawen Zheng, Yanzhuo Yang, Baogui Xu, Shuai Zhang, Falei Yuan, Zuisu Yang
Summary: This study found that monkfish peptides can improve high-fat diet-induced NAFLD by modulating the AMPK and Nrf2 pathways to enhance the liver's antioxidant capacity.
Editorial Material
Biochemistry & Molecular Biology
Jie Lu, Li Dong, Magdalene K. Montgomery
Summary: Fasting induces physiological changes in peripheral tissues, such as the liver, by suppressing the expression and activity of SREBP-1 to conserve glucose for maintaining blood glucose levels. Yoshinori Takeuchi and colleagues provide insights into the regulatory mechanism of SREBP-1 expression during fasting, highlighting the importance of the hypothalamic-pituitary-adrenal axis and glucocorticoid-induced binding of the glucocorticoid receptor to enhancer regions of the KLF15 gene.
Review
Chemistry, Multidisciplinary
Wen-sheng Yang, Jing-lin Wang, Wei Wu, Guang-fei Wang, Jun Yan, Qing Liu, Xiao-yan Wu, Qing-tong Zhou, De-hua Yang, Ming-Wei Wang, Zhi-ping Li
Summary: Inflammatory bowel disease (IBD) is a global health burden, and the current treatment mainly relies on anti-inflammatory drugs. However, their clinical efficacy and adverse reactions are still unacceptable. Resolution, as an active and orchestrated phase of inflammation, involves specialized pro-resolving mediators (SPMs), neutrophils, and phagocyte efferocytosis. The formyl peptide receptor 2 (FPR2/ALX), a human G protein-coupled receptor, can bind SPMs and participate in the resolution process.
ACTA PHARMACOLOGICA SINICA
(2023)
Article
Biotechnology & Applied Microbiology
Qilang He, Jinjie Wu, Jia Ke, Qiang Zhang, Wanyi Zeng, Zhanhao Luo, Junli Gong, Yuan Chen, Zhen He, Ping Lan
Summary: Inflammatory bowel disease (IBD) is a predisposing factor for colitis-associated cancer (CAC). The association between bile acids and the gut microbiota has been demonstrated in colon neoplasia; however, the effect of ursodeoxycholic acid (UDCA) on gut microbiota alteration in development of colitis and CAC is unknown. Our analysis of publicly available data-sets demonstrated the association of UDCA treatment and accumulation of Akkermansia. UDCA-mediated alleviation of DSS-induced colitis was microbially dependent. UDCA treatment significantly upregulated Akkermansia colonization in a mouse model. Colonization of Akkermansia was associated with enhancement of the mucus layer upon UDCA treatment as well as activation of bile acid receptors in macrophages. UDCA played a role in CAC prevention and treatment in the AOM-DSS and ApcMin/+-DSS models through downregulation of inflammation and accumulation of Akkermansia. This study suggests that UDCA intervention could reshape intestinal gut homeostasis, facilitating colonization of Akkermansia and preventing and treating colitis and CAC.
Article
Cell Biology
Jody Groenendyk, Konstantin Stoletov, Tautvydas Paskevicius, Wenjuan Li, Ning Dai, Myriam Pujol, Erin Busaan, Hoi Hei Ng, Aristeidis E. E. Boukouris, Bruno Saleme, Alois Haromy, Kaisa Cui, Miao Hu, Yanan Yan, Rui Zhang, Evangelos Michelakis, Xing-Zhen Chen, John D. D. Lewis, Jingfeng Tang, Luis B. B. Agellon, Marek Michalak
Summary: Elevation of SLC2A5 gene expression is associated with increased metastatic risk in cancer. Silencing SLC2A5 gene inhibits cancer cell proliferation, migration, and metastasis, and alters mitochondrial architecture and function. SLC2A5 is thus an important therapeutic target in cancer metastasis.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Xue Wang, Han Cheng, Jing Zhao, Jiuming Li, Ying Chen, Kaisa Cui, Lu Tian, Jia Zhang, Chaoqun Li, Shengbai Sun, Yuyang Feng, Surui Yao, Zehua Bian, Shenglin Huang, Bojian Fei, Zhaohui Huang
Summary: DLGAP1-AS2 promotes tumorigenesis and metastasis in colorectal cancer by interacting with ELOA and degrading ELOA. It also decreases LHPP expression by inhibiting ELOA-mediated transcriptional activation, thus blocking LHPP-dependent suppression of the AKT signaling pathway. DLGAP1-AS2 is bound and stabilized by CPSF2 and CSTF3.
Article
Biochemistry & Molecular Biology
Kaisa Cui, Liang Gong, Han Zhang, Ying Chen, Bingxin Liu, Zhicheng Gong, Jiuming Li, Yuanben Wang, Shengbai Sun, Yajun Li, Qiang Zhang, Yulin Cao, Qilin Li, Bojian Fei, Zhaohui Huang
Summary: This study reveals that the RNA exosome gene (EXOSC8) promotes colorectal cancer (CRC) tumorigenesis by regulating cancer-related ribosome biogenesis in CRC. Silencing of EXOSC8 decreases levels of nucleolar proteins and proliferation markers, as well as rRNA/DNA and global protein syntheses. EXOSC8 knockdown triggers ribosomal stress, releasing nucleolar protein RPL5/11 into the nucleoplasm and hijacking Mdm2 to block its E3 ubiquitin ligase function, thereby releasing and activating p53. EXOSC8 may serve as a potential therapeutic target in CRC.
Article
Oncology
Qiang Zhang, Kaisa Cui, Xiaoya Yang, Qilang He, Jing Yu, Li Yang, Gang Yao, Weiwei Guo, Zhanhao Luo, Yugeng Liu, Yuan Chen, Zhen He, Ping Lan
Summary: This study systematically evaluated the expression patterns, genetic alterations, and clinical relevance of 168 metabolic rate-limiting enzymes in human cancers and found that a subset of enzymes is closely correlated with the oncogene c-Myc. Using inosine monophosphate dehydrogenase 1 (IMPDH1) as an example, the study demonstrated that it is highly upregulated in colorectal cancer and promotes tumor growth by altering GTP metabolic reprogramming. Therefore, inhibition of IMPDH1 may be a potential treatment option for cancer.
CLINICAL AND TRANSLATIONAL MEDICINE
(2023)
Article
Oncology
Junlong Zhuang, Lan Shen, Meiqian Li, Jingya Sun, Jiange Hao, Jiaxuan Li, Zhen Zhu, Shuning Ge, Dianzheng Zhang, Hongqian Guo, Ruimin Huang, Jun Yan
Summary: Cancer-associated fibroblasts (CAF) promote cancer stemness and chemoresistance in urothelial bladder cancer (UBC) by overexpressing miR-146a-5p. MiR-146a-5p also enhances UBC stemness and chemoresistance by targeting ARID1A and PRKAA2 mRNA in UBC cells. Elevated levels of exosomal miR-146a-5p in UBC patients' serum are associated with tumor stage and relapse risk.
Editorial Material
Biochemistry & Molecular Biology
Han Han, Wenqi Wang
Summary: In a recent study published in The EMBO Journal, Qi et al (2023) propose a new model for the Hippo kinase cascade, shedding light on the long-standing question of its precise organization.
Correction
Cell Biology
Qiang Zhang, Xiaoya Yang, Jinjie Wu, Shubiao Ye, Junli Gong, Wai Ming Cheng, Zhanhao Luo, Jing Yu, Yugeng Liu, Wanyi Zeng, Chen Liu, Zhizhong Xiong, Yuan Chen, Zhen He, Ping Lan
Article
Cell Biology
Qiang Zhang, Xiaoya Yang, Jinjie Wu, Shubiao Ye, Junli Gong, Wai Ming Cheng, Zhanhao Luo, Jing Yu, Yugeng Liu, Wanyi Zeng, Chen Liu, Zhizhong Xiong, Yuan Chen, Zhen He, Ping Lan
Summary: Metabolic enzyme ACOX1 suppresses colorectal cancer progression by regulating palmitic acid reprogramming. ACOX1 is highly downregulated in CRC, and its depletion promotes cell proliferation and tumor growth while overexpression inhibits tumor growth. DUSP14 dephosphorylates ACOX1, leading to increased levels of ACOX1 substrate palmitic acid.
Article
Gastroenterology & Hepatology
Chen Liu, Junli Gong, Qiang Zhang, Guangyuan Chen, Shengmei Yin, Zhanhao Luo, Wanyi Zeng, Jing Yu, Ping Lan, Zhen He
Summary: This study demonstrates that excessive dietary iron intake perturbs diet-microbiota-epithelium interactions, leading to the initiation of intestinal tumors. The gut microbiota modulated by excessive dietary iron promotes colorectal tumorigenesis by increasing the permeability of the gut barrier and causing leakage of lumen bacteria. Epithelial cells respond to the leaked bacteria by releasing more secretory leukocyte protease inhibitor (SLPI), which acts as a pro-tumorigenic factor by activating the MAPK signaling pathway. Furthermore, the depletion of Akkermansiaceae in the gut microbiota due to excessive dietary iron can be attenuated by supplementation with Akkermansia muciniphila.
Editorial Material
Biochemistry & Molecular Biology
Yali Lu, Yan Lin, Xiaoyang Zhang, Jun Yan, Zhe Kong, Lu Zhang, Chenji Wang, Yan Huang, Shimin Zhao, Yao Li
Article
Oncology
Yong Zhang, Kaisa Cui, Yaoxiang Yang, Bingxin Liu, Minzheng Zhu, Hanqing Chen, Chong Zhao, Youlian Zhou, Yuqiang Nie
Summary: This study identified a unique CD8+CD274+ cell subpopulation associated with tumor progression and poor survival in hepatocellular carcinoma (HCC). The prognostic significance of CD274 in HCC was found to depend on CD8A expression. The high-risk subpopulation with high CD8A expression coupled with intense CD274 expression showed more mutations, higher immune response activity, and enrichment of cancer-related biological processes. Additionally, this subpopulation demonstrated increased sensitivity to immune checkpoint inhibitors.
JOURNAL OF HEPATOCELLULAR CARCINOMA
(2023)
Article
Biochemistry & Molecular Biology
Peng Teng, Kaisa Cui, Surui Yao, Bojian Fei, Feng Ling, Chaoqun Li, Zhaohui Huang
Summary: In this study, researchers found that ME2 is highly expressed in human colorectal cancer (CRC) tissues and its knockdown inhibits CRC cell proliferation. They also discovered that SIRT5 can desuccinylate ME2, activating its enzymatic activity. Activated ME2 enhances mitochondrial respiration, supporting cell proliferation and tumor development. Additionally, the levels of succinylated ME2 and SIRT5 are associated with patient prognosis.
CELL DEATH AND DIFFERENTIATION
(2023)
