Role of circular RNA cdr1as in modulation of macrophage phenotype

González, Carolina; Cimini, Maria; Cheng, Zhongjian; Benedict, Cindy; Wang, Chunlin; Trungcao, May; Mallaredy, Vandana; Rajan, Sudarsan; Garikipati, Venkata Naga Srikanth; Kishore, Raj

doi:10.1016/j.lfs.2022.121003

Cited by 9 publications

(4 citation statements)

References 61 publications

(90 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with our findings, loss of Cdr1as in brain tissues upregulates immediate-early response genes such as Fos, Arc, and Egrs, and affects brain functions such as excitatory synaptic transmission and neuropsychiatric-like alteration in the behavior of Cdr1as -/mice (21). Cdr1as also modulates the inflammatory phenotype in macrophages (37) and enhances differentiation of goat skeletal muscle satellite cells (38). However, opposing evidence also exists supporting proproliferative and oncogenic properties for Cdr1as, primarily in studies conducted in cultured cancer cells.…”

Section: Discussionsupporting

confidence: 91%

Circular RNA Cdr1as inhibits proliferation and delays injury-induced regeneration of the intestinal epithelium

Chung,

Xiao,

Han

et al. 2024

JCI Insight

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 91%

Circular RNA Cdr1as inhibits proliferation and delays injury-induced regeneration of the intestinal epithelium

Chung,

Xiao,

Han

et al. 2024

JCI Insight

View full text Add to dashboard Cite

“…Suppressed p21 expression implies that cell stress is relieved, thus leading to a reduction in macrophage infiltration in tissues. The TGF-β/p-smad3 pathway plays pivotal roles in cardiac damage induced by DOX [28], and tissue-resident macrophages secrete pro-inflammatory and fibrotic factors, such as TGF-β1, which can promote the activation of stromal cells, synthesis of collagen and release of cytokines like TNF-α and IL-1 in chronic inflammatory conditions, which contribute to EMT [62,63]. In vivo, we found that supplementing NMN suppresses the TGF-β/p-smad3 pathway and reduces macrophage infiltration.…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Wen,

Xu,

Wei

et al. 2024

IJMS

View full text Add to dashboard Cite

Doxorubicin (DOX) is a potent chemotherapeutic agent known for its multi-organ toxicity, especially in the heart, which limits its clinical application. The toxic side effects of DOX, including DNA damage, oxidative stress, mitochondrial dysfunction and cell apoptosis, are intricately linked to the involvement of nicotinamide adenine dinucleotide (NAD+). To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs. NMN treatment alleviated both multi-organ fibrosis and mortality in mice. Mechanistically, tissue fibrosis, macrophage infiltration and DOX-related cellular damage, which are potentially implicated in the development of multi-organ fibrosis, could be attenuated by NAD+ restoration. Our findings provide compelling evidence for the benefits of NMN supplementation in mitigating the adverse effects of chemotherapeutic drugs on multiple organs.

show abstract

“…Another in vitro study revealed that circCdr1 overexpression enhanced the transcription of IL-10 both in naïve and pro-inflammatory macrophages (Ref. 200). CircCHST15 was recently reported to possess an oncogenic role by promoting immune escape through upregulating the expression of IL-10 and a sponging effect on miR-155 and miR-194 in lung cancer (Ref.…”

Section: The Tumour Microenvironmentmentioning

confidence: 99%

Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology

Elemam,

Mekky,

Rashid

et al. 2024

Expert Rev. Mol. Med.

View full text Add to dashboard Cite

The host immune system status remains an unresolved mystery among several malignancies. An immune-compromised state or smart immune-surveillance tactics orchestrated by cancer cells are the primary cause of cancer invasion and metastasis. Taking a closer look at the tumour-immune microenvironment, a complex network and crosstalk between infiltrating immune cells and cancer cells mediated by cytokines, chemokines, exosomal mediators and shed ligands are present. Cytokines such as interleukins can influence all components of the tumour microenvironment (TME), consequently promoting or suppressing tumour invasion based on their secreting source. Interleukin-10 (IL-10) is an interlocked cytokine that has been associated with several types of malignancies and proved to have paradoxical effects. IL-10 has multiple functions on cellular and non-cellular components within the TME. In this review, the authors shed the light on the regulatory role of IL-10 in the TME of several malignant contexts. Moreover, detailed epigenomic and pharmacogenomic approaches for the regulation of IL-10 were presented and discussed.

show abstract

Role of circular RNA cdr1as in modulation of macrophage phenotype

Cited by 9 publications

References 61 publications

Circular RNA Cdr1as inhibits proliferation and delays injury-induced regeneration of the intestinal epithelium

Circular RNA Cdr1as inhibits proliferation and delays injury-induced regeneration of the intestinal epithelium

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology

Contact Info

Product

Resources

About