miR-498 inhibits autophagy and M2-like polarization of tumor-associated macrophages in esophageal cancer via MDM2/ATF3

Li, Dezhi; Yan, Min; Sun, Fengfei; Jun-mei, Song; Xing-sheng, HU; Yu, Sijia; Tang, Lina; Deng, Shumin

doi:10.2217/epi-2020-0341

Cited by 18 publications

(8 citation statements)

References 49 publications

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“…31 miR-498 inhibits M2 polarization of TAM by MDM2/ATF3. 32 miR-149 inhibits metastasis in breast cancer cells by limiting CSF-1-dependent recruitment and M2 polarization of macrophages. 33 In other words, our experiments revealed that miR-27a-3p targets the ATF3/ CSF-1 pathway to limit the development of NSCLS.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of inflammation and infiltration of M2 macrophages in NSCLC through the ATF3/CSF1 axis: Role of miR‐27a‐3p

Zhou,

Xu,

et al. 2023

Int J Experimental Path

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Non‐small cell lung cancer (NSCLC) imposes a significant economic burden on patients and society due to its low overall cure and survival rates. Tumour‐associated macrophages (TAM) affect tumour development and may be a novel therapeutic target for cancer. We collected NSCLC and tumour‐adjacent tissue samples. Compared with the tumour‐adjacent tissues, the Activation Transcription Factor 3 (ATF3) and Colony Stimulating Factor 1 (CSF‐1) were increased in NSCLC tissues. Levels of ATF3 and CSF‐1 were identified in different cell lines (HBE, A549, SPC‐A‐1, NCI‐H1299 and NCI‐H1795). Overexpression of ATF3 in A549 cells increased the expression of CD68, CD206 and CSF‐1. Moreover, levels of CD206, CD163, IL‐10 and TGF‐β increased when A549 cells were co‐cultured with M0 macrophages under the stimulation of CSF‐1. Using the starbase online software prediction and dual‐luciferase assays, we identified the targeting between miR‐27a‐3p and ATF3. Levels of ATF3, CSF‐1, CD206, CD163, IL‐10 and TGF‐β decreased in the miR‐27a mimics, and the tumour growth was slowed in the miR‐27a mimics compared with the mimics NC group. Overall, the study suggested that miR‐27a‐3p might inhibit the ATF3/CFS1 axis, regulate the M2 polarization of macrophages and ultimately hinder the progress of NSCLC. This research might provide a new therapeutic strategy for NSCLC.

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Section: Discussionmentioning

confidence: 99%

“…Molecularly distinct tumours can be analysed by specific miRNA for cancer diagnosis, prognosis and treatment 31 . miR‐498 inhibits M2 polarization of TAM by MDM2/ATF3 32 . miR‐149 inhibits metastasis in breast cancer cells by limiting CSF‐1‐dependent recruitment and M2 polarization of macrophages 33 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of inflammation and infiltration of M2 macrophages in NSCLC through the ATF3/CSF1 axis: Role of miR‐27a‐3p

Zhou,

Xu,

et al. 2023

Int J Experimental Path

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“…It has been reported that M2 macrophages play a preventive role in the progression of AS, the ATF3 activation appears to exert macrophage polarization into an anti-inflammatory phenotype in AS. However, Li et al recently proposed that the reduced M2-like polarization of macrophages mediated by miR-489 is associated with ATF3 deubiquitination through MDM2 ( 76 ). These findings suggest that ATF3 has a complex role in macrophage polarization.…”

Section: The Function and Molecular Mechanism Of Atf3 In Asmentioning

confidence: 99%

ATF3 and its emerging role in atherosclerosis: a narrative review

Wu¹,

Zhou²,

Xiang³

et al. 2022

Cardiovasc Diagn Ther

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Background and Objective: Atherosclerosis (AS), is characterized by the subintima lipid accumulation and chronic inflammation inside the arterial wall, causing much mortality and morbidity worldwide.Activating transcription factor 3 (ATF3) is a member of ATF/cAMP-responsive element-binding (CREB) family of transcription factors, which acts as a master regulator of adaptive response. Recent studies have indicated the implicated role of ATF3 in atherogenesis and AS progression due to its impact on metabolic disorder, vascular injury, plaque formation, and stability. In this review, we summarize the current advances in the mechanism of ATF3 activation and the contribution of ATF3 in AS, highlighting vascular intrinsic and extrinsic mechanisms of how ATF3 influences the pathology of AS. Methods:The relevant literature (from origin to March 2022) was retrieved through PubMed research to explore the regulatory mechanism of ATF3 and the specific role of ATF3 in AS. Only English publications were reviewed in this paper.Key Content and Findings: ATF3 acts as a key regulator of AS progression, which not only directly affects atherosclerotic lesions by regulating vascular homeostasis, but also gets involved in AS through systemic glucolipid metabolism and inflammatory response. The two different promoters, transcript variants, and post-translational modification in distinct cell types partly contribute to the regulatory diversity of ATF3 in AS.Conclusions: ATF3 is a crucial transcription regulatory factor during atherogenesis and AS progression.Gaining a better understanding of how ATF3 affects vascular, metabolic, and immune homeostasis would advance the progress of ATF3-targeted therapy in AS.

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“…The study presented by Li and collaborators proves the role of miR-498 in the regulation of autophagy in M2 macrophages in esophageal cancer. In this model, the inhibition of MDM2 (mouse double minute 2 homolog)-mediated ATF3 (cyclic AMP-dependent transcription factor) degradation by miR-498 led to both autophagy and the suppression of M2 polarization [ 132 ].…”

Section: Promising Therapiesmentioning

confidence: 99%

The Role of miRNA in Regulating the Fate of Monocytes in Health and Cancer

et al. 2022

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Monocytes represent a heterogeneous population of blood cells that provide a link between innate and adaptive immunity. The unique potential of monocytes as both precursors (e.g., of macrophages) and effector cells (as phagocytes or cytotoxic cells) makes them an interesting research and therapeutic target. At the site of a tumor, monocytes/macrophages constitute a major population of infiltrating leukocytes and, depending on the type of tumor, may play a dual role as either a bad or good indicator for cancer recovery. The functional activity of monocytes and macrophages derived from them is tightly regulated at the transcriptional and post-transcriptional level. This review summarizes the current understanding of the role of small regulatory miRNA in monocyte formation, maturation and function in health and cancer development. Additionally, signatures of miRNA-based monocyte subsets and the influence of exogenous miRNA generated in the tumor environment on the function of monocytes are discussed.

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miR-498 inhibits autophagy and M2-like polarization of tumor-associated macrophages in esophageal cancer via MDM2/ATF3

Cited by 18 publications

References 49 publications

Inhibition of inflammation and infiltration of M2 macrophages in NSCLC through the ATF3/CSF1 axis: Role of miR‐27a‐3p

Inhibition of inflammation and infiltration of M2 macrophages in NSCLC through the ATF3/CSF1 axis: Role of miR‐27a‐3p

ATF3 and its emerging role in atherosclerosis: a narrative review

The Role of miRNA in Regulating the Fate of Monocytes in Health and Cancer

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