Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control

Chen, Qiao Yi; Marais, Thomas Des; Costa, Max

doi:10.1093/carcin/bgz020

Cited by 23 publications

(17 citation statements)

References 111 publications

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“…Moreover, expression levels of miRNAs may be not associated with their regulatory activities. 47 For example, miR-34c-5p and its target STAB2 were both down-regulated in CRC tissues, 48 implicating that interactions between miRNAs and their targets may be more intricate. The mechanisms for the discrepancy of miR-1165-3p and the target PPM1A in asthma warrant further research.…”

Section: Discussionmentioning

confidence: 99%

MiR-1165-3p Suppresses Th2 Differentiation via Targeting IL-13 and PPM1A in a Mouse Model of Allergic Airway Inflammation

Wang

Chen

et al. 2020

Allergy Asthma Immunol Res

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Purpose CD4 + T cells are essential in the pathogenesis of allergic asthma. We have previously demonstrated that microRNA-1165-3p (miR-1165-3p) was significantly reduced in T-helper type (Th) 2 cells and that miR-1165-3p was a surrogate marker for atopic asthma. Little is known about the mechanisms of miR-1165-3p in the regulation of Th2-dominated allergic inflammation. We aimed to investigate the associations between Th2 differentiation and miR-1165b-3p in asthma as well as the possible mechanisms. Methods CD4 + naïve T cells were differentiated into Th1 or Th2 cells in vitro . MiR-1165-3p was up-regulated or down-regulated using lentiviral systems during Th1/Th2 differentiation. In vivo , the lentiviral particles with the miR-1165-3p enhancer were administered by tail vein injection on the first day of a house dust mite -induced allergic airway inflammation model. Allergic inflammation and Th1/Th2 differentiation were routinely monitored. To investigate the potential targets of miR-1165-3p, biotin-microRNA pull-down products were sequenced, and the candidates were further verified with a dual-luciferase reporter assay. The roles of a target protein phosphatase, Mg 2+ /Mn 2+ -dependent 1A (PPM1A), in Th2 cell differentiation and allergic asthma were further explored. Plasma PPM1A was determined by ELISA in 18 subjects with asthma and 20 controls. Results The lentivirus encoding miR-1165-3p suppressed Th2-cell differentiation in vitro . In contrast, miR-1165-3p silencing promoted Th2-cell development. In the HDM-induced model of allergic airway inflammation, miR-1165-3p up-regulation was accompanied by reduced airway hyper-responsiveness, serum immunoglobulin E, airway inflammation and Th2-cell polarization. IL-13 and PPM1A were the direct targets of miR-1165-3p. The expression of IL-13 or PPM1A was inversely correlated with that of miR-1165-3p. PPM1A regulated the signal transducer and activator of transcription and AKT signaling pathways during Th2 differentiation. Moreover, plasma PPM1A was significantly increased in asthmatic patients. Conclusions MiR-1165-3p negatively may regulate Th2-cell differentiation by targeting IL-13 and PPM1A in allergic airway inflammation.

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Section: Discussionmentioning

confidence: 99%

MiR-1165-3p Suppresses Th2 Differentiation via Targeting IL-13 and PPM1A in a Mouse Model of Allergic Airway Inflammation

Wang

Chen

et al. 2020

Allergy Asthma Immunol Res

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“…For instance, miR-888 promotes the spread of cancer to the body via metastasis and invasion (Li et al, 2019b). miR-31, miR-34, miR-182, miR-211, and miR-599 expression are positively correlated with Satb2 in carcinogenesis (Chen et al, 2019). miR-206 reduces Pax3 and Met gene expression and leads to the reduction of malignancy of osteosarcoma (Zhan et al, 2019).…”

Section: Noncoding Rna-based Therapies In Cancer and Modulation Of Meis And Its Partner Expressionmentioning

confidence: 99%

Oncogenic and tumor suppressor function of MEIS and associated factors

2020

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MEIS proteins are historically associated with tumorigenesis, metastasis, and invasion in cancer. MEIS and associated PBX-HOX proteins may act as tumor suppressors or oncogenes in different cellular settings. Their expressions tend to be misregulated in various cancers. Bioinformatic analyses have suggested their upregulation in leukemia/lymphoma, thymoma, pancreas, glioma, and glioblastoma, and downregulation in cervical, uterine, rectum, and colon cancers. However, every cancer type includes, at least, a subtype with high MEIS expression. In addition, studies have highlighted that MEIS proteins and associated factors may function as diagnostic or therapeutic biomarkers for various diseases. Herein, MEIS proteins and associated factors in tumorigenesis are discussed with recent discoveries in addition to how they could be modulated by noncoding RNAs or newly developed small-molecule MEIS inhibitors.

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“…MiRNAs have been evidenced to participate in a multitude of cellular activities, including cell fate determination, proliferation, apoptosis, immune response circadian rhythm, viral replication, hormone secretion, etc. [24,[31][32][33][34][35]. For example, miR-29a plays a crucial role in the dysregulation of metabolism and inflammatory signaling linked to NAFLD severity and progression [36].…”

Section: Biogenesis and Function Of Mirnasmentioning

confidence: 99%

Association of Exosomal miR-210 with Signaling Pathways Implicated in Lung Cancer

Chen

Xie

2021

Genes

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MicroRNA is a class of non-coding RNA involved in post-transcriptional gene regulation. Aberrant expression of miRNAs is well-documented in molecular cancer biology. Extensive research has shown that miR-210 is implicated in the progression of multiple cancers including that of the lung, bladder, colon, and renal cell carcinoma. In recent years, exosomes have been evidenced to facilitate cell–cell communication and signaling through packaging and transporting active biomolecules such as miRNAs and thereby modify the cellular microenvironment favorable for lung cancers. MiRNAs encapsulated inside the lipid bilayer of exosomes are stabilized and transmitted to target cells to exert alterations in the epigenetic landscape. The currently available literature indicates that exosomal miR-210 is involved in the regulation of various lung cancer-related signaling molecules and pathways, including STAT3, TIMP-1, KRAS/BACH2/GATA-3/RIP3, and PI3K/AKT. Here, we highlight major findings and progress on the roles of exosomal miR-210 in lung cancer.

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Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control

Cited by 23 publications

References 111 publications

MiR-1165-3p Suppresses Th2 Differentiation via Targeting IL-13 and PPM1A in a Mouse Model of Allergic Airway Inflammation

MiR-1165-3p Suppresses Th2 Differentiation via Targeting IL-13 and PPM1A in a Mouse Model of Allergic Airway Inflammation

Oncogenic and tumor suppressor function of MEIS and associated factors

Association of Exosomal miR-210 with Signaling Pathways Implicated in Lung Cancer

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