MicroRNA-155 governs SHIP-1 expression and localization in NK cells and regulates subsequent infiltration into murine AT3 mammary carcinoma

Kandell, Wendy; Donatelli, Sarah S.; Trinh, Thu Le; Calescibetta, Alexandra; So, Tina; Tu, Nhan; Gilvary, Danielle L.; Chen, Xianghong; Cheng, Pingyan; Adams, William A.; Chen, Yin-Kai; Liu, Jinhong; Djeu, Julie Y.; Wei, Sheng; Eksioglu, Erika A.

doi:10.1371/journal.pone.0225820

Cited by 13 publications

(17 citation statements)

References 43 publications

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“…In the searching for the most prominent targets of miR-155 in odontoblast, our bioinformatics results con rmed that SHIP1 was one of the most important factors in dental in ammation. Many reports have stated that SHIP1 is a key factor for miR-155 regulation in in ammation, brosis, and other immune processes [14,21,35]. We veri ed that miR-155 directly interacted and regulated the expression of SHIP1 in pulpal in ammation.…”

Section: Discussionmentioning

confidence: 65%

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

Guo

et al. 2021

Preprint

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Pulpitis is a commonly seen oral inflammation condition in clinical practice, it can cause much pain for the patient and may induce infections in other systems. Much is still unknown for the pathogenic mechanism of pulpitis. In this work, we discovered that the expression of miR-155 was associated with dental pulpal inflammation both in vivo and in vitro. Experiments on odontoblast cell line MDPC-23 showed miR-155 could act as a positive regulator by increasing the production of pro-inflammatory cytokines IL-1β and IL-6 during inflammatory responses, whereas knockdown of miR-155 can reverse the effects. Bioinformatics analysis demonstrated that SHIP1 is a direct target of miR-155 in odontoblasts, this result was further verified at both mRNA and protein level. Inhibition of miR-155 resulted in the downregulation of inflammation factors, while co-transfection of si-SHIP1 and miR-155 inhibitor promoted the inflammatory responses. Treatment with miR-155 mimic or si-SHIP1 up-regulated the protein level of p-PI3K and p-AKT. By contrast, miR-155 inhibitor exerted the opposite effects. miR-155 mimics could upregulated the gene expression of IL-1β and IL-6. Co-transfection of LY294002 and miR-155 mimic attenuated the inflammatory responses. Consistent with in vitro results, miR-155-/- mice could alleviate inflammatory response, as well as decrease the activation of p-PI3K and p-AKT, whereas increase the activation of SHIP1. In conclusion, these data revealed a novel role for miR-155 in regulation of dental pulpal inflammatory response by targeting SHIP1 through PI3K/AKT signaling pathway.

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Section: Discussionmentioning

confidence: 65%

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

Guo

et al. 2021

Preprint

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“…Recent studies have identi ed miR-155 as critical regulators in various physiological and pathologic processes, including hematopoietic stem-progenitor cells differentiation, in ammation, infections, and immune process of cancer formation [19,20,21]. The different functions of miR-155 in different tissues, is calling for studies to identify its role in particular circumstances.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1

Guo

et al. 2022

Mol Biol Rep

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Pulpitis is a commonly seen oral in ammation condition in clinical practice, it can cause much pain for the patient and may induce infections in other systems. Much is still unknown for the pathogenic mechanism of pulpitis. In this work, we discovered that the expression of miR-155 was associated with dental pulpal in ammation both in vivo and in vitro. Experiments on odontoblast cell line MDPC-23 showed miR-155 could act as a positive regulator by increasing the production of pro-in ammatory cytokines IL-1β and IL-6 during in ammatory responses, whereas knockdown of miR-155 can reverse the effects. Bioinformatics analysis demonstrated that SHIP1 is a direct target of miR-155 in odontoblasts, this result was further veri ed at both mRNA and protein level. Inhibition of miR-155 resulted in the downregulation of in ammation factors, while co-transfection of si-SHIP1 and miR-155 inhibitor promoted the in ammatory responses. Treatment with miR-155 mimic or si-SHIP1 up-regulated the protein level of p-PI3K and p-AKT. By contrast, miR-155 inhibitor exerted the opposite effects. miR-155 mimics could upregulate the gene expression of IL-1β and IL-6. Co-transfection of LY294002 and miR-155 mimic attenuated the in ammatory responses. Consistent with in vitro results, miR-155 −/− mice could alleviate in ammatory response, as well as decrease the activation of p-PI3K and p-AKT, whereas increase the activation of SHIP1. In conclusion, these data revealed a novel role for miR-155 in regulation of dental pulpal in ammatory response by targeting SHIP1 through PI3K/AKT signaling pathway.

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“…It is suggested that miR-155 may promote chemotaxis by regulating the receptors of CCL2 on NK cells. 204 In mesenchymal stem cells, Sirt1, the closest mammalian homolog of yeast Sir2, promoted the expression of CXCL10, which then recruited NK cells to effectively inhibit tumor growth. 205 CXCL12, a chemokine secreted by hepatic stellate cells, induced NK cell quiescence through its receptor, CXCR4, promoting breast cancer outgrowth.…”

Section: Trafficking Of Nk Cells Into Tumorsmentioning

confidence: 99%

Natural killer cell homing and trafficking in tissues and tumors: from biology to application

Ran

Lin

Tian

et al. 2022

Sig Transduct Target Ther

125

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Natural killer (NK) cells, a subgroup of innate lymphoid cells, act as the first line of defense against cancer. Although some evidence shows that NK cells can develop in secondary lymphoid tissues, NK cells develop mainly in the bone marrow (BM) and egress into the blood circulation when they mature. They then migrate to and settle down in peripheral tissues, though some special subsets home back into the BM or secondary lymphoid organs. Owing to its success in allogeneic adoptive transfer for cancer treatment and its “off-the-shelf” potential, NK cell-based immunotherapy is attracting increasing attention in the treatment of various cancers. However, insufficient infiltration of adoptively transferred NK cells limits clinical utility, especially for solid tumors. Expansion of NK cells or engineered chimeric antigen receptor (CAR) NK cells ex vivo prior to adoptive transfer by using various cytokines alters the profiles of chemokine receptors, which affects the infiltration of transferred NK cells into tumor tissue. Several factors control NK cell trafficking and homing, including cell-intrinsic factors (e.g., transcriptional factors), cell-extrinsic factors (e.g., integrins, selectins, chemokines and their corresponding receptors, signals induced by cytokines, sphingosine-1-phosphate (S1P), etc.), and the cellular microenvironment. Here, we summarize the profiles and mechanisms of NK cell homing and trafficking at steady state and during tumor development, aiming to improve NK cell-based cancer immunotherapy.

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MicroRNA-155 governs SHIP-1 expression and localization in NK cells and regulates subsequent infiltration into murine AT3 mammary carcinoma

Cited by 13 publications

References 43 publications

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1

Natural killer cell homing and trafficking in tissues and tumors: from biology to application

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