A Feedback Loop between MicroRNA 155 (miR-155), Programmed Cell Death 4, and Activation Protein 1 Modulates the Expression of miR-155 and Tumorigenesis in Tongue Cancer

Zargar, Shabir Ahmad; Tomar, Vivek Singh; Shyamsundar, Vidyarani; Ramshankar, Vijayalakshmi; Somasundaram, Kumaravel; Karunagaran, Devarajan

doi:10.1128/mcb.00410-18

Cited by 16 publications

(12 citation statements)

References 44 publications

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“…Although the miRNAs were selected because of their modulation of inflammation, several of them exhibited other, perhaps independent, actions related to tumor promotion and progression. In fact, several molecules listed have been classified as oncomiRs, such as miR-21, miR-23a, miR-29, miR-106b, miR-125b, miR-155, and miR-182 [ 316 , 362 , 363 , 364 ].…”

Section: Modulation Of the Network By Noncoding Rnas An Emergingmentioning

confidence: 99%

Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks

Hardeland

2019

IJMS

256

187

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Aging and various age-related diseases are associated with reductions in melatonin secretion, proinflammatory changes in the immune system, a deteriorating circadian system, and reductions in sirtuin-1 (SIRT1) activity. In non-tumor cells, several effects of melatonin are abolished by inhibiting SIRT1, indicating mediation by SIRT1. Melatonin is, in addition to its circadian and antioxidant roles, an immune stimulatory agent. However, it can act as either a pro- or anti-inflammatory regulator in a context-dependent way. Melatonin can stimulate the release of proinflammatory cytokines and other mediators, but also, under different conditions, it can suppress inflammation-promoting processes such as NO release, activation of cyclooxygenase-2, inflammasome NLRP3, gasdermin D, toll-like receptor-4 and mTOR signaling, and cytokine release by SASP (senescence-associated secretory phenotype), and amyloid-β toxicity. It also activates processes in an anti-inflammatory network, in which SIRT1 activation, upregulation of Nrf2 and downregulation of NF-κB, and release of the anti-inflammatory cytokines IL-4 and IL-10 are involved. A perhaps crucial action may be the promotion of macrophage or microglia polarization in favor of the anti-inflammatory phenotype M2. In addition, many factors of the pro- and anti-inflammatory networks are subject to regulation by microRNAs that either target mRNAs of the respective factors or upregulate them by targeting mRNAs of their inhibitor proteins.

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Section: Modulation Of the Network By Noncoding Rnas An Emergingmentioning

confidence: 99%

Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks

Hardeland

2019

IJMS

256

187

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“…Elevated expression of hypoxia-inducible factor-1 α (HIF-1 α ) increases trophoblastic apoptosis by regulating FOXO3a [ 35 ]. Furthermore, the correlation of miR-155 and FOXO3 was previously reported in tumors as follows: expression of miR-155 is upregulated in tumors and acts as an oncogene in cancer [ 36 , 37 ], while expression of FOXO3 is downregulated and can inhibit the development of tumors [ 38 , 39 ]. A recent study by Cai et al [ 40 ] not only showed that FOXO3 overexpression promotes trophoblast cell proliferation, migration, invasion, and inhibits apoptosis but also demonstrated that the miR-155/FOXO3 axis is involved in the suppressive effects of Baicalin on the progression of PE.…”

Section: Discussionmentioning

confidence: 99%

Methylation Mediated Silencing of miR-155 Suppresses the Development of Preeclampsia In Vitro and In Vivo by Targeting FOXO3

Luo

Pan

Guo

et al. 2022

Mediators of Inflammation

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Preeclampsia (PE) is a common pregnancy-related syndrome characterized by chronic immune activation. This study is aimed at exploring the role of miR-155 in the inflammatory pathogenesis of PE. Placental tissues and peripheral blood were collected from all subjects. BSP detection analysis was performed to evaluate miR-155 methylation levels. ELISA was performed to measure the levels of inflammatory cytokines and MMP2 in serum samples and cellular supernatants. HTR-8/SVneo and JEG-3 cells were transfected with miR-155 mimic and the inhibitor to establish the overexpressed miR-155 and silenced miR-155 cell models, respectively. Treatment with 5-Aza was performed to alter the DNA methylation level of miR-155. The PE rat model was established after subcutaneous injection of NG-nitro-L-arginine methyl ester. The CCK-8 assay, TUNEL staining, and Transwell assay were performed. Reverse transcription-quantitative PCR, Western blot analysis, and immunohistochemical assay were used to analyze related gene expression levels. The luciferase reporter assay was used to investigate the direct interaction between FOXO3 and miR-155. Results showed that miR-155 was remarkably upregulated and inversely correlated with the promoter methylation level in the placental tissue from PE patients. The in vitro experiments indicated that miR-155 decreased viability, migration, and invasion, but increased apoptosis in trophoblast cells. FOXO3 was confirmed as the target of miR-155. Transfection of the miR-155 inhibitor suppressed inflammation and oxidative stress, but elevated proliferation, migration, and invasion of trophoblast cells, which were abolished by 5-Aza treatment or cotransfection with si-FOXO3. In summary, our data suggested that methylation-mediated silencing of miR-155 can inhibit the apoptosis, inflammation, and oxidative stress of trophoblast cells by upregulating FOXO3.

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“…In fact, expression of miR-155 is regulated by a feedback circuit between Pdcd4, AP-1, and miR-155. Up-regulation of miR-155 results in progression of this type of cancer ( 78 ). Table 6 shows the interaction between miRNAs and PDCD in head and neck cancers.…”

Section: Mirnas and Pdcdmentioning

confidence: 99%

Interplay Between Non-Coding RNAs and Programmed Cell Death Proteins

et al. 2022

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Programmed cell death (PDCD) family of proteins includes at least 12 members, function of seven of them being more investigated. These members are PDCD1, PDCD2, PDCD4, PDCD5, PDCD6, PDCD7 and PDCD10. Consistent with the important roles of these proteins in the regulation of apoptosis, dysregulation of PDCDs is associated with diverse disorders ranging from intervertebral disc degeneration, amyotrophic lateral sclerosis, immune thrombocytopenia, type 1 diabetes, congenital hypothyroidism, Alzheimer’s disease to different types of cancers. More recently, the interaction between non-coding RNAs and different members of PDCD family is being discovered. In the current study, we described the functional interactions between PDCDs and two classes of non-coding RNAs, namely microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). miR-21 and miR-183 are two miRNAs whose interactions with PDCDs have been assessed in different contexts. The lncRNAs interaction with PDCDs is mainly assessed in the context of neoplasia indicating the role of MALAT1, MEG3, SNHG14 and LINC00473 in this process.

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A Feedback Loop between MicroRNA 155 (miR-155), Programmed Cell Death 4, and Activation Protein 1 Modulates the Expression of miR-155 and Tumorigenesis in Tongue Cancer

Cited by 16 publications

References 44 publications

Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks

Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks

Methylation Mediated Silencing of miR-155 Suppresses the Development of Preeclampsia In Vitro and In Vivo by Targeting FOXO3

Interplay Between Non-Coding RNAs and Programmed Cell Death Proteins

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