Total cardiolipin levels in gastric and colon cancer: evaluating the prognostic potential

Lipids in Health and Disease, Journal Year: 2025, Volume and Issue: 24(1)

Published: Feb. 27, 2025

Cardiolipin (CL) is a signature phospholipid of mitochondria that maintains the integrity mitochondrial membrane and supports proper function. Alterations in CL level composition can impair or, conversely, improve function bioenergetics, both which are critical for cancer metabolism. However, conflicting reports on levels across different types limited research using human patient samples limit our understanding its diagnostic potential. This cross-sectional study explores concentrations gastric colon tissues CL-specific fluorescent probe MitoCLue compares them to adjacent healthy tissues. In cancer, showed no significant differences between tumor tissues, suggesting metabolic shifts do not affect total content. contrast, exhibited 33% increase levels, indicating adaptation and/or mass cancer. No associations were found demographic factors; although weak correlation with body index was noted. We successfully applied quantitatively assess from patients or The distinct suggest there cancer-type specific adaptations, reflecting unique bioenergetic demands reprogramming pathways. While observed compared this modest variation may utility as standalone biomarker.

Language: Английский

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Knockdown of SLC7A5 inhibits malignant progression and attenuates oxaliplatin resistance in gastric cancer by suppressing glycolysis

Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)

Published: March 25, 2025

Abstract Background Chemotherapy resistance is a major challenge in the treatment of intermediate and advanced gastric cancer (GC). This study aimed to recognize oxaliplatin resistance-related genes (OXARGs) GC explore their role mechanism GC. Methods OXARGs with prognostic value were analyzed using data from GEO TCGA databases. RT-qPCR WB assay applied verify expression MT2A, NOTCH1 SLC7A5 oxaliplatin-resistant cells (HGC27R MKN45R). The effect on malignant phenotype was verified by CCK-8, EDU, TUNEL, colony formation, wound healing, transwell assay, tumor bearing experiments assay. Results Bioinformatics analysis experimental validation indicate that target for oxaliplatin-resistance Knockdown obviously decreased viability, migration, invasion vitro growth vivo. It also increased apoptosis levels BAX expression, reduced BCL2, MMP 2 MMP9. Additionally, knockdown enhanced sensitivity both Furthermore, downregulated HK2, LDHA, Glut1, PDK1 vivo vitro, leading extracellular glucose lactate levels. However, glutathione significantly attenuated regulatory cells. Trial registration Not Applicable. Conclusion inhibits progression attenuates suppressing glycolysis.

Language: Английский

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Advances in the Study of Metabolic Reprogramming in Gastric Cancer

Cancer Medicine, Journal Year: 2025, Volume and Issue: 14(10)

Published: May 1, 2025

ABSTRACT Background Gastric cancer is one of the most prevalent malignancies digestive system and associated with a poor prognosis, particularly in advanced metastatic stages, where 5‐year survival rate significantly low. Methods Recent research has demonstrated that metabolic reprogramming—including alterations glucose, lipid, amino‐acid metabolism—plays critical role both development progression this disease. To gain deeper insights into these shifts, scientists have increasingly employed metabolomics, non‐invasive technique detects quantifies small molecules within cancerous tissues, thereby enhancing prognostic assessments. Aim Analyzing profiles gastric‐cancer tissues can reveal significant changes key pathways, which may open new avenues for targeted therapies ultimately improve patient outcomes. Conclusion This article reviews recent advancements study reprogramming gastric cancer, aiming to identify potential therapeutic targets offer hope patients.

Language: Английский

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A Potential Oncogenic Role for PFKFB3 Overexpression in Gastric Cancer Progression

Clinical and Translational Gastroenterology, Journal Year: 2021, Volume and Issue: 12(7), P. e00377 - e00377

Published: July 1, 2021

OBJECTIVES: PFKFB3 regulates glycolysis in tumor cells, might function as an oncogene, and is associated with cancer metastasis. However, its role gastric (GC) remains largely unknown. METHODS: expression was assessed by immunohistochemistry (IHC) GC tissues paired paracancerous histological normal (PCHNTs). The associations of clinical features HIF-1α, Ki-67, E-cadherin, Snail, Vimentin levels were assessed. A series vivo vitro experiments performed to investigate the effects on growth, migration, invasion cells. RESULTS: We found that significantly higher compared PCHNTs ( P = 0.000). positively correlated size 0.000), differentiation 0.025), venous 0.084), nerve 0.014), lymphatic local invasive depth nodal metastasis tumor-node-metastasis stage patient survival Notably, upregulation highly increased epithelial-mesenchymal transition (EMT) samples. overexpression modulated cell proliferation, EMT cells , concomitant activation NF-κB signaling. Administration inhibitor attenuated PFKFB3-induced promoted development nude mice, which PFK-15, a inhibitor. DISCUSSION: could potentiate malignancy through pathway–mediated EMT, suggesting represents potential target for therapy.

Language: Английский

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Pyrolyzed deketene curcumin controls regulatory T cell generation and gastric cancer metabolism cooperate with 2-deoxy-d-glucose

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 6, 2023

Pyrolyzed deketene curcumin GO-Y022 prevents carcinogenesis in a gastric cancer mouse model. However, it is still less clear if affects tumor-induced immune suppression. In this study, we found that inhibited Treg generation the presence of transforming growth factor beta 1 (TGF-β). showed impact on Foxp3+ Tregs tumor microenvironment. Gastric cells produce large amount L-lactate and diminish inhibitory role against response to TGF-β. Therefore, naïve CD4+ T co-cultured with treated increased generation. GO-Y022-induced cell death was further enhanced by 2-deoxy-d-glucose (2DG), glycolysis inhibitor. Combination treatment 2DG results reduced production cells. Overall, GO-Y022-treatment restricted glucose metabolism inhibits survival promotes anti-tumor immunity.

Language: Английский

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