YYFZBJS Inhibits Colorectal Tumorigenesis by Remodeling Gut Microbiota and Influence on M2 Macrophage Polarization  &lt;i&gt;in vivo&lt;/i&gt; and  &lt;i&gt;in vitro&lt;/i&gt;

Chai, Ningli; Cheng, Yuelei; Xiong, Ye; Shi, Wenfei; Yao, Yiqing; Sui, Hua; Zhu, Hong-Jian

doi:10.2139/ssrn.3837225

Cited by 7 publications

(9 citation statements)

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“…In addition, multiple studies suggest that M2 macrophages contribute to NSCLC progression by promoting invasion (Li et al., 2020; Sumitomo et al., 2019; Wei et al., 2017). Arg‐1, CD206 and IL‐10 are key M2 macrophage markers (Chai et al., 2021). Through detection of their expression, the current research has found that lentinan can inhibit the M2 polarization of tumor‐associated macrophages.…”

Section: Discussionmentioning

confidence: 99%

Lentinan inhibits cell invasion via M2 polarization of tumor‐associated macrophages and Wnt/β‐catenin signaling in non‐small cell lung cancer

Yang,

Cheng,

et al. 2024

Chem Biol Drug Des

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Non‐small cell lung cancer (NSCLC) is an aggressive and devastating cancer due to its metastasis induced by increased invasion. Lentinan is a polysaccharide exerting antitumor roles in multiple cancers, including lung cancer. However, the influence of lentinan on cell invasion in NSCLC remains unclear. Cell invasion was detected by transwell analysis. Matrix metallopeptidase 9 (MMP9) levels were measured through immunofluorescence staining. The markers arginase‐1 (Arg‐1), CD206 and interleukin (IL)‐10 (IL‐10) of M2 macrophages, Wnt3a, and β‐catenin levels were measured by western blot or enzyme linked immunosorbent assay. Lentinan did not affect cell viability and proliferation in NSCLC cells. Lentinan suppressed cell invasion and reduced the expression and secretion of MMP9. Lentinan attenuated also M2 polarization of tumor‐associated macrophages. Moreover, lentinan mitigated the M2 macrophage conditioned medium‐mediated cell invasion and MMP9 alterations in NSCLC cells. Lentinan inhibited the activation of the Wnt/β‐catenin signaling in NSCLC cells. The activated Wnt/β‐catenin pathway reversed the suppressive effects of lentinan on cell invasion and MMP9 level in NSCLC cells. In conclusion, lentinan reduces cell invasion in NSCLC cells by inhibiting the M2 polarization of tumor‐associated macrophages and the Wnt/β‐catenin signaling.

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Section: Discussionmentioning

confidence: 99%

Lentinan inhibits cell invasion via M2 polarization of tumor‐associated macrophages and Wnt/β‐catenin signaling in non‐small cell lung cancer

Yang,

Cheng,

et al. 2024

Chem Biol Drug Des

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“…The procedures for inducing the CAC model using AOM and DSS were implemented as previously outlined [ 21 ]. Mice, aged 5–6 weeks, were subjected to intraperitoneal injection with a single dose of AOM (Merck, Darmstadt, Germany), followed by one-week exposure to 2.5% DSS (MP Biomedicals, Solon, OH, USA) in drinking water.…”

Section: Methodsmentioning

confidence: 99%

YTE-17 inhibits colonic carcinogenesis by resetting antitumor immune response via Wnt5a/JNK mediated metabolic signaling

Sui,

Deng,

Chai

et al. 2024

Journal of Pharmaceutical Analysis

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“…The imbalance of ETBF stimulates STAT3-mediated polarization of M2 macrophages to promote malignant transformation of adenomas, thus promoting the occurrence and development of CAC. By inhibiting ETBF imbalance, YYFZBJS inhibits M2 polarization and plays an antitumor role in CAC ( 113 ). Ganoderma lucidum polysaccharide (GLP) is a component of Ganoderma lucidum, which reduce intestinal macrophage infiltration, down-regulate the expression of inflammatory factors such as IL-1 β, and attenuate the tumorigenesis of CAC ( 114 ).…”

Section: Drugs That Regulate Cac Through Macrophagesmentioning

confidence: 99%

Roles of macrophages on ulcerative colitis and colitis-associated colorectal cancer

Zhang

et al. 2023

Front. Immunol.

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Colitis-associated colorectal cancer is the most serious complication of ulcerative colitis. Long-term chronic inflammation increases the incidence of CAC in UC patients. Compared with sporadic colorectal cancer, CAC means multiple lesions, worse pathological type and worse prognosis. Macrophage is a kind of innate immune cell, which play an important role both in inflammatory response and tumor immunity. Macrophages are polarized into two phenotypes under different conditions: M1 and M2. In UC, enhanced macrophage infiltration produces a large number of inflammatory cytokines, which promote tumorigenesis of UC. M1 polarization has an anti-tumor effect after CAC formation, whereas M2 polarization promotes tumor growth. M2 polarization plays a tumor-promoting role. Some drugs have been shown to that prevent and treat CAC effectively by targeting macrophages.

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YYFZBJS Inhibits Colorectal Tumorigenesis by Remodeling Gut Microbiota and Influence on M2 Macrophage Polarization <i>in vivo</i> and <i>in vitro</i>

Cited by 7 publications

References 0 publications

Lentinan inhibits cell invasion via M2 polarization of tumor‐associated macrophages and Wnt/β‐catenin signaling in non‐small cell lung cancer

Lentinan inhibits cell invasion via M2 polarization of tumor‐associated macrophages and Wnt/β‐catenin signaling in non‐small cell lung cancer

YTE-17 inhibits colonic carcinogenesis by resetting antitumor immune response via Wnt5a/JNK mediated metabolic signaling

Roles of macrophages on ulcerative colitis and colitis-associated colorectal cancer

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