Interleukin-6 and Interleukin-8 Regulate STAT3 Activation Migration/Invasion and EMT in Chrysophanol-Treated Oral Cancer Cell Lines

Hsu, Po-Yang; Chen, Yi‐Hsuan; Cheng, Ching‐Feng; Kuo, Chan‐Yen; Sytwu, Huey‐Kang

doi:10.3390/life11050423

Cited by 18 publications

(11 citation statements)

References 56 publications

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“…CXCL8 enhances the stemness properties of the self-renewal capability, expression of stemness-related genes, and tumorigenicity in small-cell lung cancer sphere-forming cells [ 128 ]. IL-6 and CXCL8 promote EMT and cell invasion through STAT3 signaling in oral cancer [ 129 ]. Snail is a key transcriptional repressor of E-cadherin that induces EMT and promotes tumor progression.…”

Section: Cxcl8-cxcr1/2 Signaling Pathwaymentioning

confidence: 99%

Roles of the CXCL8-CXCR1/2 Axis in the Tumor Microenvironment and Immunotherapy

Han

Yang

et al. 2021

Molecules

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In humans, Interleukin-8 (IL-8 or CXCL8) is a granulocytic chemokine with multiple roles within the tumor microenvironment (TME), such as recruiting immunosuppressive cells to the tumor, increasing tumor angiogenesis, and promoting epithelial-to-mesenchymal transition (EMT). All of these effects of CXCL8 on individual cell types can result in cascading alterations to the TME. The changes in the TME components such as the cancer-associated fibroblasts (CAFs), the immune cells, the extracellular matrix, the blood vessels, or the lymphatic vessels further influence tumor progression and therapeutic resistance. Emerging roles of the microbiome in tumorigenesis or tumor progression revealed the intricate interactions between inflammatory response, dysbiosis, metabolites, CXCL8, immune cells, and the TME. Studies have shown that CXCL8 directly contributes to TME remodeling, cancer plasticity, and the development of resistance to both chemotherapy and immunotherapy. Further, clinical data demonstrate that CXCL8 could be an easily measurable prognostic biomarker in patients receiving immune checkpoint inhibitors. The blockade of the CXCL8-CXCR1/2 axis alone or in combination with other immunotherapy will be a promising strategy to improve antitumor efficacy. Herein, we review recent advances focusing on identifying the mechanisms between TME components and the CXCL8-CXCR1/2 axis for novel immunotherapy strategies.

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Section: Cxcl8-cxcr1/2 Signaling Pathwaymentioning

confidence: 99%

Roles of the CXCL8-CXCR1/2 Axis in the Tumor Microenvironment and Immunotherapy

Han

Yang

et al. 2021

Molecules

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“…The elevated gene expression for E and E+1 materials is a result of physiological processes, whereas no proapoptotic proliferation inhibition of HaCaT or NHDF was observable. The interleukins IL6 and IL8 are also markers of proliferation and healthy cell communication, which could manifest during contact tests with used materials …”

Section: Resultsmentioning

confidence: 99%

Polyurethane-Based Nanocomposites for Regenerative Therapies of Cancer Skin Surgery with Low Inflammatory Potential to Healthy Fibroblasts and Keratinocytes In Vitro

Mrówka,

Lenża-Czempik,

Dawicka

et al. 2023

ACS Omega

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Nanocomposites based on thermoplastic polyurethanes (TPUs) filled with halloysite nanotubes (HNTs) were studied for their physicochemical and biological properties. Nanocomposites containing halloysite nanotube filler contents of 1 and 2% (E+1 and E+2), respectively, were obtained by extrusion. The newly formed E+1 and E+2 nanomaterials exhibited better flexibility and similar thermal properties compared to neat polyurethane. The use of atomic force microscopy (AFM) and differential scanning calorimetry (DSC) thermogram analysis showed that the distribution of halloysite nanotubes in the polymer matrix is more evenly dispersed in the E+1 nanomaterial, where the grains in the E+2 nanomaterial have a greater tendency to form agglomerates. Mechanical tests have shown that nanocomposites with the addition of HNT are characterized by a higher stress at break and elongation at break compared to neat TPU. The results of cytotoxicity tests suggest that the nanocomposite materials express lower toxicity to normal HaCaT and NHDF than to cancer Me45 cells. Further studies showed that the tested materials induced the expression of proinflammatory interleukins IL6 and IL8 in normal cells, but their overexpression in the cancer cell line resulted in cytostatic effects and proliferation reduction. Such a conclusion suggests the possible application of tested materials for regenerative therapies in cancer surgeries.

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“…Chrysophanol downregulated Bcl‐2 and upregulated Bax and cytochrome c , confirming that chrysophanol‐induced apoptosis was mitochondria‐dependent. As a natural anthraquinone, the apoptosis‐inducing effects of chrysophanol on a broad range of human cancer cells, including breast (Ren et al., 2018), oral (Hsu & Chen, 2021), cervical (Trybus & Król, 2021), ovarian (Lim et al., 2018) and colorectal (Deng et al., 2020) cancer cells, have been reported. Here, we demonstrated the effects of chrysophanol on gastric cancer cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Chrysophanol induces apoptosis and ferroptosis of gastric cancer cells by targeted regulation of mTOR

Xi,

Ding,

Weng

et al. 2024

Chem Biol Drug Des

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Programmed cell death (PCD) induction is a promising strategy for killing gastric cancer cells. In this study, we investigated the effects of chrysophanol on apoptosis and ferroptosis in gastric cancer cells. Chrysophanol in concentrations ranging from 0 to 100 μM were used to treat GES‐1, HGC‐27 and AGS cells. Cell counting kit‐8 assay, colony formation assay, 5‐ethynyl‐2′‐deoxyuridine staining, flow cytometry, JC‐1 probe insertion, dihydroethidium staining and western blotting were performed. The effects of chrysophanol on gastric cancer cells were evaluated in vivo using a xenograft mouse model. Chrysophanol had no cytotoxic effects on GES‐1 cells. Chrysophanol with concentrations higher than 25 μM inhibited gastric cancer cell colony formation and proliferation. Chrysophanol induces gastric cancer cell apoptosis in a dose‐dependent manner, accompanied by mitochondrial membrane potential dysfunction and cytochrome c release. Additionally, chrysophanol increased the levels of reactive oxygen species, total iron, and Fe2+ in HGC‐27 and AGS cells, in a dose‐dependent manner. Treatment of cells with the ferroptosis inhibitor ferrostatin‐1 attenuated the effects of chrysophanol on cell survival and the expression of ferroptosis markers SLC7A11 and GPX4. Screening by GEO software indicated that the mTOR signalling pathway is possibly regulated by chrysophanol. Furthermore, mTOR overexpression significantly reversed the inhibitory effects of chrysophanol on gastric cancer cells. In gastric cancer xenograft mouse models, chrysophanol treatment inhibited tumour growth and downregulated SLC7A11 and GPX4. Chrysophanol induces apoptosis and ferroptosis, making it a potential candidate for killing gastric cancer cells. The beneficial effects of chrysophanol may be attribute to the targeted regulation of mTOR.

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Interleukin-6 and Interleukin-8 Regulate STAT3 Activation Migration/Invasion and EMT in Chrysophanol-Treated Oral Cancer Cell Lines

Cited by 18 publications

References 56 publications

Roles of the CXCL8-CXCR1/2 Axis in the Tumor Microenvironment and Immunotherapy

Roles of the CXCL8-CXCR1/2 Axis in the Tumor Microenvironment and Immunotherapy

Polyurethane-Based Nanocomposites for Regenerative Therapies of Cancer Skin Surgery with Low Inflammatory Potential to Healthy Fibroblasts and Keratinocytes In Vitro

Chrysophanol induces apoptosis and ferroptosis of gastric cancer cells by targeted regulation of mTOR

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