Physalin B attenuates liver fibrosis via suppressing LAP2α‐HDAC1 mediated deacetylation of glioma‐associated oncogene 1 and hepatic stellate cell activation

Weiskirchen, Ralf

doi:10.1111/bph.15588

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…HDAC1 is also highly expressed in glioma tissues, and high expression of glioma is related to the proliferation, migration, invasion, angiogenesis, and poor prognosis of glioma cells [ 29 ]. In addition, it has been suggested that increased activation of HDAC1/2/6 and Sp1 is the basis of glioblastoma drug resistance and tumor growth [ 30 ]. We also found elevated HDAC1 expression in glioma tissues, which is associated with poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analyses reveal the role of histone deacetylase genes in prognosis and immune response in low-grade glioma

Shen

et al. 2022

PLoS ONE

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Many studies have shown that Histone deacetylases (HDAC) is involved in the occurrence of malignant tumors and regulates the occurrence, proliferation, invasion, and migration of malignant tumors through a variety of signaling pathways. In the present, we explored the role of Histone deacetylases genes in prognosis and immune response in low-grade glioma. Using consensus clustering, we built the new molecular clusters. Using HDAC genes, we constructed and validated the prognostic model in two independent cohort datasets. Patients were divided into high-risk and low-risk groups. Then, we explored the molecular characteristics, clinical characteristics, tumor microenvironment and immune infiltration levels of two clusters and risk groups. Receiver operating characteristic analyses were built for model assessment. We finally detected the expression levels of signature genes between tumor and normal tissues. Low-grade can be separated into two molecular clusters using 11 HDACs genes. Two clusters had different clinical characteristics and prognosis. Nex, we constructed a prognosis model using six HDAC genes (HDAC1, HDAC4, HDAC5, HDAC7, HDAC9, and HDAC10), which was also validated in an independent cohort dataset. Furthermore, multivariate cox regression indicated that the calculated risk score was independently associated with prognosis in low-grade glioma, and risk score can predict the five-year survival probability of low-grade glioma well. High-risk patients can be attributed to multiple complex function and molecular signaling pathways, and the genes alterations of high- and low-risk patients were significantly different. We also found that different survival outcomes of high- and low- risk patients could be involved in the differences of immune filtration level and tumor microenvironment. Subsequently, using signature genes, we identified several small molecular compounds that could be useful for low-grade glioma patients’ treatment. Finally, we detected the expression levels of signature genes in tumor tissues. our study uncovers the biology function role of HDAC genes in low-grade glioma. We identified new molecular subtypes and established a prognostic model based on six HDAC genes, which was well applied in two independent cohort data. The regulation of HDAC genes in low-grade glioma involved in multiple molecular function and signaling pathways and immune infiltration levels. Further experiments in vivo and vitro were required to confirm the present findings.

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Section: Discussionmentioning

confidence: 99%

Comprehensive analyses reveal the role of histone deacetylase genes in prognosis and immune response in low-grade glioma

Shen

et al. 2022

PLoS ONE

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“…In liver fibrosis, the extracellular matrix (ECM) is excessively produced and abnormally deposited. [ 1,2 ] At present, it is suggested that the activation and proliferation of hepatic stellate cells (HSCs) are the central links in liver fibrosis. [ 3 ] Moreover, an increasing number of studies have indicated that macrophages play an important role in liver fibrosis, and M1 polarization of macrophages can secrete a large amount of proinflammatory factors to promote the abnormal activation and tissue inflammatory response of HSCs.…”

Section: Introductionmentioning

confidence: 99%

TWEAK promotes inflammatory response in liver fibrosis

Kong,

Yang,

et al. 2023

J Biochem & Molecular Tox

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This study aimed to investigate the role and mechanism of tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) in liver fibrosis. The liver Kupffer cells (KCs) and mononuclear macrophages (J774A.1) were used as the objects of study to induce M1 polarization with LPS/IFN‐γ. After TWEAK intervention, the M1 cell proportion and marker cytokine levels were detected. Thereafter, CD266 expression was silenced, and NLRP3 expression was inhibited by the NLRP3 inhibitor, so as to investigate the impact of TWEAK on M1 polarization of KCs. In addition, the mouse model of liver fibrosis was constructed to observe the influence of TWEAK on mouse liver fibrosis. According to our results, TWEAK promoted M1 polarization of liver KCs and J774A.1 cells, and silencing CD266 expression or treatment with the NLRP3 inhibitor suppressed the effect of TWEAK. In the mouse experiment, it was discovered that after knocking down NLRP3 expression or using NLRP3 inhibitor to antagonize the effect of TWEAK, the mouse liver function and M1 cell level in liver tissues were improved.

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Inhibition of long noncoding RNA Gm41724 alleviates pressure overload-induced cardiac fibrosis by regulating lamina-associated polypeptide 2α

Kong

Zhou

et al. 2023

Pharmacological Research

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Physalin B attenuates liver fibrosis via suppressing LAP2α‐HDAC1 mediated deacetylation of glioma‐associated oncogene 1 and hepatic stellate cell activation

Cited by 4 publications

References 5 publications

Comprehensive analyses reveal the role of histone deacetylase genes in prognosis and immune response in low-grade glioma

Comprehensive analyses reveal the role of histone deacetylase genes in prognosis and immune response in low-grade glioma

TWEAK promotes inflammatory response in liver fibrosis

Inhibition of long noncoding RNA Gm41724 alleviates pressure overload-induced cardiac fibrosis by regulating lamina-associated polypeptide 2α

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