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:10.21203/rs.3.rs-19746/v2

Cited by 16 publications

(24 citation statements)

References 35 publications

(39 reference statements)

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“…Monocytes from blood differentiate to M1 or M2 subtype macrophages, depending on their interactions with other cells present in tissues (Figures 6 and 7). Such differentiation is dependent on the environmental stimuli these cells are subject to (183)(184)(185)(186)(187)(188)(189)(190). The first type of antimicrobial macrophage activation became known as M1 macrophages (191).…”

Section: Polarization Of Macrophagesmentioning

confidence: 99%

CAFs Interacting With TAMs in Tumor Microenvironment to Enhance Tumorigenesis and Immune Evasion

Günaydın

2021

Front. Oncol.

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Cancer associated fibroblasts (CAFs) and tumor associated macrophages (TAMs) are among the most important and abundant players of the tumor microenvironment. CAFs as well as TAMs are known to play pivotal supportive roles in tumor growth and progression. The number of CAF or TAM cells is mostly correlated with poor prognosis. Both CAFs and TAMs are in a reciprocal communication with the tumor cells in the tumor milieu. In addition to such interactions, CAFs and TAMs are also involved in a dynamic and reciprocal interrelationship with each other. Both CAFs and TAMs are capable of altering each other’s functions. Here, the current understanding of the distinct mechanisms about the complex interplay between CAFs and TAMs are summarized. In addition, the consequences of such a mutual relationship especially for tumor progression and tumor immune evasion are highlighted, focusing on the synergistic pleiotropic effects. CAFs and TAMs are crucial components of the tumor microenvironment; thus, they may prove to be potential therapeutic targets. A better understanding of the tri-directional interactions of CAFs, TAMs and cancer cells in terms of tumor progression will pave the way for the identification of novel theranostic cues in order to better target the crucial mechanisms of carcinogenesis.

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Section: Polarization Of Macrophagesmentioning

confidence: 99%

CAFs Interacting With TAMs in Tumor Microenvironment to Enhance Tumorigenesis and Immune Evasion

Günaydın

2021

Front. Oncol.

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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: 96%

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 can disrupt the crosstalk between cancer cells and tumor-associated macrophages through IL-6R/STAT3 signaling, thereby inhibiting epithelial-mesenchymal transition. Studies have found that CPEB3 is related to the tumorigenesis and development of glioma [25], high-grade serous ovarian cancer [26], colorectal cancer [27], hepatocellular carcinoma [28], cervical cancer [29]. Based on the two hub RBPs trained by the TARGET cohort, multi-step Cox regression analysis produced a riskscore model that can predict the prognosis of NB.…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of RNA binding protein-associated prognostic model for Neuroblastoma

Yang

Zhou

et al. 2021

Preprint

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Background: The abnormal expression of RNA binding protein (RBP) may be related to the development and progress of cancer. However, little is known about the mechanism of RBP in neuroblastoma (NB). Methods: We downloaded the RNA expression data of NB and normal nervous tissues from the (TARGET) database and GTEx database, and determined the differential expression of RBP between normal and cancerous tissues. Then the function and prognostic value of these RBPs were systematically studied. Results: A total of 348 differentially expressed RBPs were identified, together with 166 up-regulated RBPs and 182 down-regulated RBPs. Two hub RBPs (CPEB3 and CTU1) were identified as prognostic-related genes and chose to build prognostic risk score models. Further analysis showed that based on this model, the overall survival rate of patients in the high-risk subgroup was lower (P=2.152e-04). The area under the curve(AUC) of the receiver-operator characteristic curve(ROC) of the prognostic model is 0.720 in the TARGET cohort. There is a significant difference in the survival rate of patients in the high and low risk subgroups in the validation data set GSE85047 (P = 0.1237e-08), the AUC is 0.730. Conclusions: RNA binding protein (CPEB3 and CTU1) can be used as molecular markers of NB. Keywords: Neuroblastoma, RNA binding proteins, prognostic, TARGET, GTEx

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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 16 publications

References 35 publications

CAFs Interacting With TAMs in Tumor Microenvironment to Enhance Tumorigenesis and Immune Evasion

CAFs Interacting With TAMs in Tumor Microenvironment to Enhance Tumorigenesis and Immune Evasion

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

Identification and validation of RNA binding protein-associated prognostic model for Neuroblastoma

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