Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment

Zou, Kejian; Wang, Yaodong; Hu, Yan; Zheng, Lei; Xu, Wei; Li, Guoxin

doi:10.1177/1010428317695962

Cited by 14 publications

(9 citation statements)

References 45 publications

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“…Immunohistochemistry and immunofluorescence were performed as described in our previous work. 26,27 The sections were deparaffinized, rehydrated, blocked with goat serum and incubated with…”

Section: Immunohistochemistry (Ihc) and Immunofluorescence(if)mentioning

confidence: 99%

Inhibition of CREB‐mediated ZO‐1 and activation of NF‐κB‐induced IL‐6 by colonic epithelial MCT4 destroys intestinal barrier function

Zhang

Wang

et al. 2019

Cell Proliferation

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Objective Inflammatory bowel disease (IBD) is a disorder intestinal inflammation and impaired barrier function, associated with increased epithelial expression of monocarboxylate transporter 4 (MCT4). However, the specific non‐metabolic function and clinical relevance of MCT4 in IBD remain to be fully elucidated. Methods Lentivirus‐mediated overexpression of MCT4 was used to assess the role of MCT4 in transcriptionally regulating ZO‐1 and IL‐6 expression by luciferase assays, WB and ChIP. IP was used to analyse the effect of MCT4 on the interaction NF‐κB‐CBP or CREB‐CBP, and these MCT4‐mediated effects were confirmed in vivo assay. Results We showed that ectopic expression of MCT4 inhibited ZO‐1 expression, while increased pro‐inflammatory factors expression, leading to destroy intestinal epithelial barrier function in vitro and in vivo. Mechanistically, MCT4 contributed NF‐κB p65 nuclear translocation and increased the binding of NF‐κB p65 to the promoter of IL‐6, which is attributed to MCT4 enhanced NF‐κB‐CBP interaction and dissolved CREB‐CBP complex, resulting in reduction of CREB activity and CREB‐mediated ZO‐1 expression. In addition, treatment of experimental colitis with MCT4 inhibitor α‐cyano‐4‐hydroxycinnamate (CHC) ameliorated mucosal intestinal barrier function, which was due to attenuation of pro‐inflammation factors expression and enhancement of ZO‐1 expression. Conclusion These findings suggested a novel role of MCT4 in controlling development of IBD and provided evidence for potential targets of IBD.

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Section: Immunohistochemistry (Ihc) and Immunofluorescence(if)mentioning

confidence: 99%

Inhibition of CREB‐mediated ZO‐1 and activation of NF‐κB‐induced IL‐6 by colonic epithelial MCT4 destroys intestinal barrier function

Zhang

Wang

et al. 2019

Cell Proliferation

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“…It is reported that p53 can inhibit Bcl-2, while it also activates Bax and Bak proteins. Bax protein tends to activate the death effect factor caspase or change the cell membrane permeability, 51 resulting in the release of small molecules and ions, by cytochrome C, through the cell membrane, therefore promoting the apoptosis of the cell. When Bcl-2 is dominant, then the change in Bcl-2/Bax can regulate apoptosis, and cell possesses antiapoptotic effects.…”

Section: ■ Discussionmentioning

confidence: 99%

Sanjie Yiliu Formula Inhibits Colorectal Cancer Growth by Suppression of Proliferation and Induction of Apoptosis

Tang

Huang

et al. 2021

ACS Omega

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Colorectal cancer (CRC) is one of the most common malignancies worldwide. As current therapies toward CRC, including chemotherapy and radiotherapy, pose limitations, such as multidrug resistance (MDR) as well as the intrinsic and potential cytotoxic effects, necessitating to find more effective treatment options with fewer side effects, traditional Chinese medicine (TCM) has an advantage in complementary therapies. In the present study, 3-(4,5-dimethylthiozol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assays), trypan blue staining, colony formation, 4,6-diamidino-2phenylindole dihydrochloride (DAPI) staining, cell cycle determination, and Annexin V-FITC/PI staining were used to examine the efficacy of Sanjie Yiliu Formula (SJYLF) against CRC proliferation and to investigate its underlying molecular mechanisms through protein expression of various proapoptotic factors by quantitative polymerase chain reaction (q-PCR) and Western blotting. This four-herb-TCM SJYLF can be suggested as one of the decoctions clinically effective in late-stage cancer treatment. Our results suggest that SJYLF robustly decreased the viability of only CRC cell lines (HCT-8, SW-480, HT-29, and DLD-1) and not the normal human kidney cells (HK-2). Moreover, SJYLF significantly suppressed proliferation and induced apoptosis in HCT-8 and downregulated cyclin D1, CDK4, and BCL-2, while Bax expression was upregulated at both mRNA and protein expression levels.

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“…What’s more, REC8 interacted with NF-κB, leading to inhibit NF-κB activity. Dynamic change NF-κB p65 activity is critical event in nucleus shuttle [ 32 ]. Depletion of REC8 expression in BGC823 cells drastically contributed the binding of NF-κB to VEGF promoter, leading VEGF transcription.…”

Section: Discussionmentioning

confidence: 99%

REC8 suppresses tumor angiogenesis by inhibition of NF-κB-mediated vascular endothelial growth factor expression in gastric cancer cells

Liu

et al. 2020

Biol Res

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Background Tumor angiogenesis is an essential event for tumor growth and metastasis. It has been showed that REC8, a component of the meiotic cohesion complex, played a vital role in Epithelial-Mesenchymal Transition (EMT) in gastric cancer. However, the role of REC8 in gastric cancer angiogenesis remains to be identified. Results Inhibition of REC8 expression in gastric cancer cells contributed to tumor angiogenesis in the gastric cancer microenvironment. The clinical analysis demonstrated that the loss of REC8 in gastric cancer with enrichment of MVD. Depletion of REC8 expression in gastric cancer cells significantly increased tube formation of human umbilical vein endothelial cells (HUVECs), which is attributed to enhancement of vascular endothelial growth factor (VEGF) secretion caused by REC8 slicing. While addition of neutralizing antibody targeted VEGF into supernatant drastically reversed the effect of REC8 loss in gastric cancer cells on tube formation. Mechanistic analyses indicated that ablation of REC8 promotes nuclear factor-κB (NF-κB) p65 activity and its downstream gene VEGF expression, leading to tube formation. Conclusions These results demonstrated a novel REC8 function that suppressed tumor angiogenesis and progression by attenuation of VEGF in gastric cancer microenvironment.

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Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment

Cited by 14 publications

References 45 publications

Inhibition of CREB‐mediated ZO‐1 and activation of NF‐κB‐induced IL‐6 by colonic epithelial MCT4 destroys intestinal barrier function

Inhibition of CREB‐mediated ZO‐1 and activation of NF‐κB‐induced IL‐6 by colonic epithelial MCT4 destroys intestinal barrier function

Sanjie Yiliu Formula Inhibits Colorectal Cancer Growth by Suppression of Proliferation and Induction of Apoptosis

REC8 suppresses tumor angiogenesis by inhibition of NF-κB-mediated vascular endothelial growth factor expression in gastric cancer cells

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