CPEB3 inhibits epithelial-mesenchymal transition by disrupting the crosstalk between colorectal cancer cells and tumor-associated macrophages via IL-6R/STAT3 signaling

Zhong, Qian; Fang, Yuxin; Lai, Qiuhua; Wang, Shanci; He, Chengcheng; Li, Aimin; Liu, Side; Yan, Qun

doi:10.1186/s13046-020-01637-4

Cited by 82 publications

(51 citation statements)

References 45 publications

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“…CCL2 production has been reported to be more inducible in HER2+/ER− breast carcinoma cells compared with HER2+/ER+ cells under EGF/HRG stimulation, and enhanced NF-kB transcription levels were detected in HER2+/ER− breast carcinoma cells (5). Emerging evidence indicates that the JAK/STAT pathway can also promote CCL2 production under stimulation (6)(7)(8)(9)(10)(11)(12)(13). Neddylation is a reversible protein modification process mediated by NEDD8.…”

Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

Jin

Lin

et al. 2021

Front. Oncol.

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Tumor microenvironment (TME) formation is a major cause of immunosuppression. The TME consists of a considerable number of macrophages and stromal cells that have been identified in multiple tumor types. CCL2 is the strongest chemoattractant involved in macrophage recruitment and a powerful initiator of inflammation. Evidence indicates that CCL2 can attract other host cells in the TME and direct their differentiation in cooperation with other cytokines. Overall, CCL2 has an unfavorable effect on prognosis in tumor patients because of the accumulation of immunosuppressive cell subtypes. However, there is also evidence demonstrating that CCL2 enhances the anti-tumor capability of specific cell types such as inflammatory monocytes and neutrophils. The inflammation state of the tumor seems to have a bi-lateral role in tumor progression. Here, we review works focusing on the interactions between cancer cells and host cells, and on the biological role of CCL2 in these processes.

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Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

Jin

Lin

et al. 2021

Front. Oncol.

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“…This mechanism was demonstrated since tumorinfiltrating CD11b + CD11c + show profound expression of IL-6 and decreased ability of T-cell stimulation [79]. Cytoplasmic polyadenylation element-binding protein 3 (CPEB3) ex-hibits a tumor-suppressive role in CRC, and has been shown to inhibit EMT by interrupting the crosstalk between CRC cells and tumor-associated macrophages, in an IL-6/STAT3dependent manner [80]. In addition, Th17 cells suppress CD8+ cell migration, which is a prerequisite for the efficacy of immunotherapy, by downregulating CXCR3 expression, through an IL-17A/STAT3 mechanism, in advanced-stage CRC patients [81].…”

Section: Stat3 In Combination With Immunotherapymentioning

confidence: 99%

Targeting STAT3 Signaling Pathway in Colorectal Cancer

Gargalionis

Papavassiliou

2021

Biomedicines

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Signal transducer and activator of transcription 3 (STAT3) is a critical transcription factor that has been firmly associated with colorectal cancer (CRC) initiation and development. STAT3 mediates key inflammatory mechanisms in colitis-associated cancer, becomes excessively activated in CRC, and enhances cancer cell proliferation, tumor growth, angiogenesis, invasion, and migration. STAT3 hyperactivation in malignant cells, surrounding immune cells and cancer-associated fibroblasts, mediates inhibition of the innate and adaptive immunity of the tumor microenvironment, and, therefore, tumor evasion from the immune system. These features highlight STAT3 as a promising therapeutic target; however, the mechanisms underlying these features have not been fully elucidated yet and STAT3 inhibitors have not reached the clinic in everyday practice. In the present article, we review the STAT3 signaling network in CRC and highlight the current notion for the design of STAT3-focused treatment approaches. We also discuss recent breakthroughs in combination immunotherapy regimens containing STAT3 inhibitors, therefore providing a new perception for the clinical application of STAT3 in CRC.

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“…CPEB3, a member of the CPEB family, was discovered to monitor cell translation by adjusting cytoplasmic polyadenylation. It has also been reported that CPEB3 was aberrantly expressed in several types of cancer ( 23 , 30 , 49 ). In a study of ovarian cancer cells, miR-301b-3p increased cell invasion and migration by targeting CPEB3 ( 50 ).…”

Section: Discussionmentioning

confidence: 88%

Long non‑coding RNA MIR22HG inhibits glioma progression by downregulating microRNA‑9/CPEB3

Nan

Yan

et al. 2020

Oncol Lett

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Glioma is one of the most common and aggressive malignant intracranial tumors worldwide. Recently, non-coding RNAs have been found to play critical roles in the development of glioma. However, the exact mechanisms have not been fully elucidated. In the present study, reverse transcription-quantitative PCR was used to determine the expression level of the long non-coding RNA MIR22HG and microRNA (miR)-9, while western blot analysis was used to detect the protein expression level of CPEB3. The potential binding sites were predicted using the StarBase v2.0 online tool and the hypothesis was verified using a luciferase reporter assay. A Cell Counting Kit-8 assay was used to assess cell viability, while wound healing and Matrigel assays were used to determine the migration and invasion ability of glioma cancer cells. The results showed that MIR22HG expression level was decreased but miR-9 expression level was elevated in glioma tissues and cell lines. Furthermore, MIR22HG was found to sponge miR-9, while CPEB3 was the direct target of miR-9 in the glioma cell line. Functionally, MIR22HG regulated the proliferation, invasion and migration of the glioma cell line by targeting miR-9. CPEB3 may be involved in the progression of the glioma cell line. Taken together, these findings confirmed that MIR22HG suppressed glioma development by inhibiting the miR-9/CPEB3 axis and provides a novel therapeutic strategy for glioma treatment.

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CPEB3 inhibits epithelial-mesenchymal transition by disrupting the crosstalk between colorectal cancer cells and tumor-associated macrophages via IL-6R/STAT3 signaling

Cited by 82 publications

References 45 publications

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

Targeting STAT3 Signaling Pathway in Colorectal Cancer

Long non‑coding RNA MIR22HG inhibits glioma progression by downregulating microRNA‑9/CPEB3

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