Publications by authors named "Yuhong Suo"

Article Synopsis
  • Aristolochic acids (AAs) are linked to an increased risk of hepatocellular carcinoma (HCC) due to their ability to influence cell death processes.
  • The study revealed that AAs interact with the p53 protein in liver cancer cells, disrupting its normal function, specifically affecting ferroptosis and the regulation of key genes like GADD45A and NRF2.
  • This interaction leads to down-regulation of GADD45A and up-regulation of NRF2, ultimately promoting tumor growth by inhibiting ferroptosis, suggesting that targeting NRF2 could be a potential therapeutic strategy for liver cancer.
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Members of the E26 transformation-specific (ETS) variant transcription factor family act as either tumor suppressors or oncogenic factors in numerous types of cancer. ETS variant transcription factor 7 (ETV7) participates in the development of malignant tumors, whereas its involvement in colorectal cancer (CRC) is less clear. In this study, The Cancer Genome Atlas (TCGA) and immunochemistry staining were applied to check the clinical relevance of ETV7 and interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in CRC patients.

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Heat shock protein family A member 8 (HSPA8) participates in the folding or degradation of misfolded proteins under stress and plays critical roles in cancer. In this study, we investigated the function of HSPA8 in the development of liver cancer. By analyzing the TCGA transcriptome dataset, we found that HSPA8 was upregulated in 134 clinical liver cancer tissue samples, and positively correlated with poor prognosis.

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Viral immune evasion is crucial to the pathogenesis of hepatitis B virus (HBV) infection. However, the role of HBV in the modulation of innate immune evasion is poorly understood. A liver-specific histone acetyltransferase 1 (Hat1) knockout (KO) mouse model and HAT1 KO cell line were established.

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The Fc fragment of IgG binding protein (FCGBP) has been confirmed to play an important role in various cancers. However, the specific role of FCGBP in hepatocellular carcinoma (HCC) remains undefined. Thus, in this study, the enrichment analyses (Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis) of FCGBP in HCC and extensive bioinformatic analyses using data of clinicopathologic characteristics, genetic expression and alterations, and immune cell infiltration were perfomed.

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Background: Liver transplantation (LT), resection (LR), and ablation (LA) are three curative-intent treatment options for patients with early hepatocellular carcinoma (HCC). We aimed to develop a prognostic calculator to compare the long-term outcomes following each of these therapies.

Methods: A total of 976 patients with HCC within the Milan criteria who underwent LT, LR, and LA between 2009 and 2019 from four institutions were evaluated.

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Background: Hepatocellular carcinoma has been identified to be among the most prevalent malignancies in the world and has an unfavorable prognosis. Immune checkpoints perform an essential function in many biological processes and are associated with the survival of cancer patients. The function of immune checkpoints remains unknown.

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The tumor suppressor gene adenomatous polyposis coli (APC) is frequently inactivated or absent in colorectal carcinoma (CRC). Loss‑of‑function of APC promotes the expression of β‑catenin, which is critical for CRC development. Since β‑catenin acts as an important transcription factor, blockage of β‑catenin may have side effects, including impairment of tissue homeostasis and regeneration, thus limiting the application of β‑catenin inhibitors for the treatment of patients with CRC.

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Nonalcoholic steatohepatitis (NASH) is a global public health challenge. Overwhelmed oxidative stress and impaired autophagy play an important role in the progression of NASH. Chemerin is an adipokine that has attracted much attention in inflammation and metabolic diseases.

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Colon cancer is one of the most common malignancies worldwide, while the molecular mechanism remains largely unknown. miR-223-3p plays an important role in cancer development. Here, we found that miR-223-3p was up-regulated in 30 cases of colon cancer tissues as compared with their adjacent normal tissues.

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