Aldo-keto reductase family 1 member B10 prevents esophageal squamous cell carcinoma from reactive carbonyl species-induced cell death and promotes its progression DOI Creative Commons
Shau-Hsuan Li, Wan‐Ting Huang, Yen‐Hao Chen

et al.

Cancer Cell International, Journal Year: 2024, Volume and Issue: 24(1)

Published: Dec. 22, 2024

Chronic alcohol consumption and tobacco usage are major risk factors for esophageal squamous cell carcinoma (ESCC). Excessive lead to oxidative stress the generation of reactive carbonyl species (RCS) which induce DNA damage apoptosis. This phenomenon contributes carcinogenesis in various organs including ESCC. However, it also raises an important question on how ESCC cells evade RCS-induced apoptosis grow rapidly under these conditions. Therefore, we hypothesize that some enzymes produced by capable catabolizing RCS, preventing neoplastic from undergoing apoptosis, potentially contributing progression. To identify significant gene clusters involved metabolism RCS ESCC, used Agilent SurePrint G3 Human V2 GE 8 × 60 K microarray kit analyze differentially expressed genes between nine paired tissues adjacent normal taken areas distant tumor site. Bioinformatics analysis using ontology (GO) was performed categorize genes. validate findings, immunohistochemical staining specimens 169 surgically resected patients then correlated with treatment outcomes. Furthermore, identified signaling pathway its biological effects were investigated lines vitro 4-nitroquinoline 1-oxide (4-NQO)-induced-ESCC murine model vivo. Interestingly, found one significantly altered 57 GO molecular function domain terms (GO:0004033 aldo-keto reductase activity; P = 0.021) tumors tissue associated metabolism. Among within this domain, AKR1B10 (aldo-keto family 1 member B10; 0.006) as most gene. Immunohistochemical revealed expression higher than epithelium. In addition, independently a poorer prognosis patients. Enzyme-linked immunosorbent assay results further demonstrated blood concentrations 72 24 healthy controls. experiments inhibiting endogenous enhanced cytotoxicity 4-hydroxy trans-2-nonenal, type RCS. 4-NQO-induced-ESCC model, oleanolic acid, inhibitor, reduced incidence tumors. Our findings suggested is independent adverse prognosticator could prevent promote be potential therapeutic strategy

Language: Английский

Fagopyrum dibotrys extract improves nonalcoholic fatty liver disease via inhibition of lipogenesis and endoplasmic reticulum stress in high-fat diet-fed mice DOI Creative Commons
Da Wang, Dan Zhang,

Ziyun Zhu

et al.

BMC Research Notes, Journal Year: 2024, Volume and Issue: 17(1)

Published: Oct. 16, 2024

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing, presenting a treatment challenge due to limited options. Endoplasmic reticulum (ER) stress and associated lipid metabolism disorders are main causes NAFLD, making it important inhibit ER for effective treatment. Fagopyrum dibotrys has hypolipidemic, anti-inflammatory hepatoprotective properties, showing promise in treating NAFLD. However, its effects on NAFLD remain unclear. This study used high-fat diet (HFD) establish mouse models supplemented with extract (FDE) evaluate therapeutic effect underlying mechanisms.

Language: Английский

Citations

0
METTL3 affects the biological function of lung adenocarcinoma through the FGF2/PI3K/AKT /mTOR pathway DOI Creative Commons
Shaoting Chen, Xiuqing shen, Pengju Cao

et al.

Frontiers in Oncology, Journal Year: 2024, Volume and Issue: 14

Published: Oct. 21, 2024

Introduction This study aims to investigate the role of m6A regulatory factor METTL3 in LUAD. Methods By examining expression LUAD and conducting cellular functional experiments, biological functions were discussed. mRNA-seq MeRIP-qPCR used identify downstream target genes pathways. Results The level is lower than that control group. downregulation promoted proliferation, migration, invasion cells, while overexpression results opposite effects. Furthermore, we found FGF2 was negatively regulated by METTL3. Inhibiting reversed tumor-promoting effects caused cells. Silencing enhanced stability mRNA. resulted reduced activity PI3K/AKT/mTOR signaling pathway knockdown Discussion In summary, our findings unveil an intricate network involving METTL3/FGF2/PI3K/AKT/mTOR provide valuable insights into molecular mechanisms underlying tumor progression, thus holding significant implications for targeted therapy advancing research.

Language: Английский

Citations

0
Aldo-keto reductase family 1 member B10 prevents esophageal squamous cell carcinoma from reactive carbonyl species-induced cell death and promotes its progression DOI Creative Commons
Shau-Hsuan Li, Wan‐Ting Huang, Yen‐Hao Chen

et al.

Cancer Cell International, Journal Year: 2024, Volume and Issue: 24(1)

Published: Dec. 22, 2024

Chronic alcohol consumption and tobacco usage are major risk factors for esophageal squamous cell carcinoma (ESCC). Excessive lead to oxidative stress the generation of reactive carbonyl species (RCS) which induce DNA damage apoptosis. This phenomenon contributes carcinogenesis in various organs including ESCC. However, it also raises an important question on how ESCC cells evade RCS-induced apoptosis grow rapidly under these conditions. Therefore, we hypothesize that some enzymes produced by capable catabolizing RCS, preventing neoplastic from undergoing apoptosis, potentially contributing progression. To identify significant gene clusters involved metabolism RCS ESCC, used Agilent SurePrint G3 Human V2 GE 8 × 60 K microarray kit analyze differentially expressed genes between nine paired tissues adjacent normal taken areas distant tumor site. Bioinformatics analysis using ontology (GO) was performed categorize genes. validate findings, immunohistochemical staining specimens 169 surgically resected patients then correlated with treatment outcomes. Furthermore, identified signaling pathway its biological effects were investigated lines vitro 4-nitroquinoline 1-oxide (4-NQO)-induced-ESCC murine model vivo. Interestingly, found one significantly altered 57 GO molecular function domain terms (GO:0004033 aldo-keto reductase activity; P = 0.021) tumors tissue associated metabolism. Among within this domain, AKR1B10 (aldo-keto family 1 member B10; 0.006) as most gene. Immunohistochemical revealed expression higher than epithelium. In addition, independently a poorer prognosis patients. Enzyme-linked immunosorbent assay results further demonstrated blood concentrations 72 24 healthy controls. experiments inhibiting endogenous enhanced cytotoxicity 4-hydroxy trans-2-nonenal, type RCS. 4-NQO-induced-ESCC model, oleanolic acid, inhibitor, reduced incidence tumors. Our findings suggested is independent adverse prognosticator could prevent promote be potential therapeutic strategy

Language: Английский

Citations

0