Publications by authors named "Guanqi Dai"

Aims: Aurora kinase A (AURKA) has been implicated in promoting myeloid and renal fibrosis. This study aimed to investigate the impact and underlying mechanism of AURKA on liver fibrosis and to assess the therapeutic potential of MLN8237, a small-molecule AURKA inhibitor, in preventing liver fibrosis in mice.

Methods: The research used bioinformatics analysis and immunohistochemistry staining on fibrotic liver tissues from human and mouse models to assess AURKA expression.

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  • Gender disparities in digestive system cancers show that females generally experience lower incidence and mortality rates than males, highlighting a potential protective role of estrogen.
  • Estrogen interacts with various estrogen receptors (ERs) and has complex effects on non-reproductive organs, which may influence the development of cancers like hepatocellular and colorectal carcinoma.
  • The review discusses mechanisms of estrogen and ERs in these cancers and suggests that understanding these pathways could lead to new treatments and preventive strategies, ultimately improving patient outcomes.
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Aim: In 2019, to examine the functions of METTL3 in liver and underlying mechanisms, we generated mice with hepatocyte-specific METTL3 homozygous knockout (METTL3Δhep) by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT) or Alb-Cre mice (JAX), respectively. In this study, we explored the potential reasons why hepatocyte-specific METTL3 homozygous disruption by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and then postnatal lethality.

Main Methods: Mice with hepatocyte-specific METTL3 knockout were generated by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT; Strain No.

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  • Scientists are studying how heat treatment (hyperthermia) can help fight nasopharyngeal cancer (NPC) and why some cancer cells resist the heat.
  • They found that using heat with a drug called oridonin makes cancer cells easier to kill, especially the tough ones that don't respond well to regular treatments.
  • The study also discovered that a protein called Cirbp helps cancer cells survive heat, and reducing Cirbp improves the effectiveness of heat treatment against these cancer cells.
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  • The study investigates the role of Mettl3, an mA "writer" protein, in liver lipid metabolism and its connection to non-alcoholic fatty liver disease (NAFLD).
  • Researchers found that lower levels of Mettl3 in the liver are linked to more severe NAFLD, and when Mettl3 was knocked out in mice, it led to increased fat accumulation and liver damage.
  • The findings suggest that Mettl3 influences lipid metabolism by regulating specific mRNA levels, highlighting its potential role in the progression of NAFLD and liver health.
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B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1) is overexpressed in various cancer types. We found that mRNA levels were elevated in nasopharyngeal carcinoma (NPC) cell lines. In immunohistochemical analyses, high Bmi-1 levels were observed in not only 5 of 38 non-cancerous nasopharyngeal squamous epithelial biopsies, but also in 66 of 98 NPC specimens (67.

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Autophagy is crucial for maintaining cellular energy homeostasis and for cells to adapt to nutrient deficiency, and nutrient sensors regulating autophagy have been reported previously. However, the role of eiptranscriptomic modifications such as mA in the regulation of starvation-induced autophagy is unclear. Here, we show that the mA reader YTHDF3 is essential for autophagy induction.

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Background: JAK1 and JAK2 have been implicated in fibrosis and cancer as a fibroblast-related marker; however, their role in liver fibrosis has not been elucidated. Here, we aim to determine the effect and underlying mechanism of JAK1/2 inhibition on liver fibrosis and hepatic stellate cells (HSCs) and further explore the therapeutic efficacy of Ruxolitinib, a JAK1/2 selective inhibitor, on preventing and reversing liver fibrosis in mice.

Methods: Immunohistochemistry staining of JAK1 and JAK2 were performed on liver tissue in mice with hepatic fibrosis and human liver tissue microarray of liver cirrhosis and liver cancer.

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In this study, we investigated the role of embryonic gene Cripto-1 (CR-1) in hepatocellular carcinoma (HCC) using hepatocyte-specific CR-1-overexpressing transgenic mice. The expression of truncated 1.7-kb CR-1 transcript (SF-CR-1) was significantly higher than the full-length 2.

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The pro-inflammatory and pro-fibrotic liver microenvironment facilitates hepatocarcinogenesis. However, the effects and mechanisms by which the hepatic fibroinflammatory microenvironment modulates intrahepatic hepatocellular carcinoma (HCC) progression and its response to systematic therapy remain largely unexplored. We established a syngeneic orthotopic HCC mouse model with a series of persistent liver injury induced by CCl gavage, which mimic the dynamic effect of hepatic pathology microenvironment on intrahepatic HCC growth and metastasis.

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The onset of liver cancer is insidious. Currently, there is no effective method for the early detection of hepatocellular carcinoma (HCC). Transcriptomic profiles of 826 tissue samples from the Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), Genotype tissue expression (GTEx), and International Cancer Genome Consortium (ICGC) databases were utilized to establish models for early detection and surveillance of HCC.

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Dexmedetomidine (DEX) is an anesthetic that is widely used in the clinic, and it has been reported to exhibit paradoxical effects in the progression of multiple solid tumors. In this study, we sought to explore the mechanism by which DEX regulates hepatocellular carcinoma (HCC) progression underlying liver fibrosis. We determined the effects of DEX on tumor progression in an orthotopic HCC mouse model of fibrotic liver.

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Long noncoding RNAs have been proved in regulating tumourigenesis, including hepatocellular carcinoma (HCC). However, up to date, the role of PCAT6 in HCC is rare to be reported. In current study, bioinformatics analysis and quantitative real-time PCR were applied to examine the expression of PCAT6 in HCC.

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