Butyrate prevents the migration and invasion, and aerobic glycolysis in gastric cancer via inhibiting Wnt/β‐catenin/c‐Myc signaling

Liang, Yufeng; Rao, Zilan; Du, Dongwei; Wang, Yiwen; Fang, Taiyong

doi:10.1002/ddr.22043

Cited by 15 publications

(8 citation statements)

References 52 publications

(67 reference statements)

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“…In lung cancer, DSTYK silencing enhances glycolysis by the Wnt/β-catenin/LDHA axis [51]. In gastric cancer, LiCl, a Wnt/β-catenin pathway activator, reverses the inhibitory effect of butyrate on aerobic glycolysis [52]. In our study, XAV-939 reversed the increase in GLUT1, HK2, LDHA, and PDK1 expression induced by IL13RA2 overexpression, suggesting that IL13RA2 enhances glycolysis of IH by activating the Wnt/βcatenin pathway.…”

Section: Discussionsupporting

confidence: 53%

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

LIU,

MA,

et al. 2024

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Background: Interleukin 13 receptor subunit alpha 2 (IL13RA2) plays an essential role in the progression of many cancers. However, the role of IL13RA2 in infantile haemangioma (IH) is still unknown. Materials and Methods: IL13RA2 expression in IH tissues was analyzed using western blot, qRT-PCR, and immunofluorescence. The role of IL13RA2 in haemangioma-derived endothelial cells (HemECs) was determined following knockdown or overexpression of IL13RA2 using CCK-8, colony formation, apoptosis, wound healing, tubule formation, Transwell, and western blot. Results: IL13RA2 expression was upregulated in IH tissues. IL13RA2 overexpression promoted proliferation, migration, and invasion of HemECs and induced glycolysis, which was confirmed with a glycolysis inhibitor. Specifically, IL13RA2 interacted with β-catenin and activated the Wnt/β-catenin pathway in HemECs, which were involved in the above-mentioned effects of IL13RA2. Conclusions: These findings revealed that targeting IL13RA2 is a potential therapeutic approach for IH.

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Section: Discussionsupporting

confidence: 53%

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

LIU,

MA,

et al. 2024

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“…evaluated the anti-tumor effect of butyrate in vitro and in vivo systems. 45 They found that butyrate inhibits proliferation, migration, and invasion of tumor cells. Furthermore, butyrate inhibited aerobic glycolysis in tumor cells via inhibiting wnt/β-catenin/c-Myc signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Gut microbiome-derived butyrate inhibits the immunosuppressive factors PD-L1 and IL-10 in tumor-associated macrophages in gastric cancer

Lee,

Jhun,

Woo

et al. 2024

Gut Microbes

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Early detection and surgical treatment are essential to achieve a good outcome in gastric cancer (GC). Stage IV and recurrent GC have a poor prognosis. Therefore, new treatments for GC are needed. We investigated the intestinal microbiome of GC patients and attempted to reverse the immunosuppression of the immune and cancer cells of GC patients through the modulation of microbiome metabolites. We evaluated the levels of programmed death-ligand 1 (PD-L1) and interleukin (IL)-10 in the peripheral blood immunocytes of GC patients. Cancer tissues were obtained from patients who underwent surgical resection of GC, and stained sections of cancer tissues were visualized via confocal microscopy. The intestinal microbiome was analyzed using stool samples of healthy individuals and GC patients. Patient-derived avatar model was developed by injecting peripheral blood mononuclear cells (PBMCs) from advanced GC (AGC) patients into NSG mice, followed by injection of AGS cells. PD-L1 and IL-10 had higher expression levels in immune cells of GC patients than in those of healthy controls. The levels of immunosuppressive factors were increased in the immune and tumor cells of tumor tissues of GC patients. The abundances of Faecalibacterium and Bifidobacterium in the intestinal flora were lower in GC patients than in healthy individuals. Butyrate, a representative microbiome metabolite, suppressed the expression levels of PD-L1 and IL-10 in immune cells. In addition, the PBMCs of AGC patients showed increased levels of immunosuppressive factors in the avatar mouse model. Butyrate inhibited tumor growth in mice. Restoration of the intestinal microbiome and its metabolic functions inhibit tumor growth and reverse the immunosuppression due to increased PD-L1 and IL-10 levels in PBMCs and tumor cells of GC patients.

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“…For example, CD36 has been reported to inhibit the glycolysis and tumorigenesis of CRC through the glypican 4-β-catenin-c-Myc signaling axis (40). Liang et al (41) indicated that butyrate controlled gastric cancer cell proliferation, migration, invasion and aerobic glycolysis by downregulating Wnt/β-catenin/c-MYC signaling. In human hepatocellular carcinoma, Gankyrin has been reported to upregulate glycolysis and glutaminolysis to promote tumorigenesis, metastasis and drug resistance via upregulating c-Myc through the activation of β-catenin signaling (26).…”

Section: Discussionmentioning

confidence: 99%

Tensin 4 facilitates aerobic glycolysis, migration and invasion of colorectal cancer cells through the β‑catenin/c‑Myc signaling pathway

Wang,

Lu,

2024

Oncol Lett

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Tensin 4 (TNS4) is overexpressed in multiple cancers, including colorectal cancer (CRC), and is associated with a poor prognosis of patients with CRC. However, the role and underlying mechanisms of TNS4 in CRC have yet to be elucidated. The expression of TNS4 in CRC tissues were analyzed by immunohistochemistry. Cell migration and invasion were assessed in vitro using Transwell assay. Western blot and reverse transcription (RT)-quantitative (q)PCR were used to investigate the molecular mechanisms by which TNS4 regulates aerobic glycolysis, migration and invasion of CRC cells. The present study demonstrated that TNS4 was highly expressed in the cancer tissues of patients with CRC and significantly associated with the tumor-node-metastasis stages. TNS4 silencing led to a significant decrease in glucose consumption and lactate production in CRC cells, and knockdown of TNS4 suppressed the migration and invasion of CRC cells via aerobic glycolysis through the β-catenin/c-Myc pathway. Notably, treatment with DASA-58, an activator of glycolysis, or SKL2001, an activator of β-catenin/c-Myc signaling, significantly reversed the effect of TNS4 knockdown on aerobic glycolysis, migration and invasion of CRC cells. Collectively, these results suggest that TNS4 may act as a novel regulator of aerobic glycolysis, migration and invasion of CRC cells by modulating β-catenin/c-Myc signaling, providing a new potential biomarker and therapeutic target in CRC.

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Butyrate prevents the migration and invasion, and aerobic glycolysis in gastric cancer via inhibiting Wnt/β‐catenin/c‐Myc signaling

Cited by 15 publications

References 52 publications

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

Gut microbiome-derived butyrate inhibits the immunosuppressive factors PD-L1 and IL-10 in tumor-associated macrophages in gastric cancer

Tensin 4 facilitates aerobic glycolysis, migration and invasion of colorectal cancer cells through the β‑catenin/c‑Myc signaling pathway

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