microRNAs (miRNAs) and DNA methylation are the 2 epigenetic modifications that have emerged in recent years as the most critical players in the regulation of gene expression. Compelling evidence has indicated the roles of miRNAs and DNA methylation in modulating cellular transformation and tumorigenesis. miRNAs act as negative regulators of gene expression and are involved in the regulation of both physiologic conditions and during diseases, such as cancer, inflammatory diseases, and psychiatric disorders, among others. Meanwhile, aberrant DNA methylation manifests in both global genome changes and in localized gene promoter changes, which influences the transcription of cancer genes. In this review, we described the mutual regulation of miRNAs and DNA methylation in human cancers. miRNAs regulate DNA methylation by targeting DNA methyltransferases or methylation-related proteins. On the other hand, both hyper- and hypo-methylation of miRNAs occur frequently in human cancers and represent a new level of complexity in gene regulation. Therefore, understanding the mechanisms underlying the mutual regulation of miRNAs and DNA methylation may provide helpful insights in the development of efficient therapeutic approaches.

https://www.tandfonline.com/doi/pdf/10.1080/15592294.2016.1273308

Mutual regulation of microRNAs and DNA methylation in human cancers.

MicroRNAs (miRNAs) are endogenous non-coding small RNAs that downregulate target gene expression by imperfect base-pairing with the 3′ untranslated regions (3′UTRs) of target gene mRNAs. MiRNAs play important roles in regulating cancer cell proliferation, stemness maintenance, tumorigenesis, cancer metastasis, and cancer therapeutic resistance. While studies have shown that dysregulation of miRNA-205-5p (miR-205) expression is controversial in different types of human cancers, it is generally observed that miR-205-5p expression level is downregulated in breast cancer and that miR-205-5p exhibits a tumor suppressive function in breast cancer. This review focuses on the role of miR-205-5p dysregulation in different subtypes of breast cancer, with discussions on the effects of miR-205-5p on breast cancer cell proliferation, epithelial–mesenchymal transition (EMT), metastasis, stemness and therapy-resistance, as well as genetic and epigenetic mechanisms that regulate miR-205-5p expression in breast cancer. In addition, the potential diagnostic and therapeutic value of miR-205-5p in breast cancer is also discussed. A comprehensive list of validated miR-205-5p direct targets is presented. It is concluded that miR-205-5p is an important tumor suppressive miRNA capable of inhibiting the growth and metastasis of human breast cancer, especially triple negative breast cancer. MiR-205-5p might be both a potential diagnostic biomarker and a therapeutic target for metastatic breast cancer.

https://www.mdpi.com/2311-553X/5/4/53/pdf

MiR-205 Dysregulations in Breast Cancer: The Complexity and Opportunities.

MicroRNA dysregulation in the tumor microenvironment influences the phenotype of pancreatic cancer.

Periodontitis is a highly prevalent chronic inflammatory disease leading to periodontal tissue breakdown and subsequent tooth loss, in which excessive host immune response accounts for most of the tissue damage and disease progression. Despite of the imperative need to develop host modulation therapy, the inflammatory responses and cell population dynamics which are finely tuned by the pathological microenvironment in periodontitis remained unclear. To investigate the local microenvironment of the inflammatory response in periodontitis, 10 periodontitis patients and 10 healthy volunteers were involved in this study. Single-cell transcriptomic profilings of gingival tissues from two patients and two healthy donors were performed. Histology, immunohistochemistry, and flow cytometry analysis were performed to further validate the identified cell subtypes and their involvement in periodontitis. Based on our single-cell resolution analysis, we identified HLA-DR-expressing endothelial cells and CXCL13+ fibroblasts which are highly associated with immune regulation. We also revealed the involvement of the proinflammatory NLRP3+ macrophages in periodontitis. We further showed the increased cell-cell communication between macrophage and T/B cells in the inflammatory periodontal tissues. Our data generated an intriguing catalog of cell types and interaction networks in the human gingiva and identified new inflammation-promoting cell subtypes involved in chronic periodontitis, which will be helpful in advancing host modulation therapy.

/pdf/single-cell-rna-sequencing-identifies-new-inflammation-uvmja8bbmc.pdf

Single-Cell RNA Sequencing Identifies New Inflammation-Promoting Cell Subsets in Asian Patients With Chronic Periodontitis.

MicroRNAs are a kind of small and non-coding RNAs, which have been demonstrated to play an important role in the progression of human cervical cancer. Here, we found that the expression of miR-205 was low in cervical cancer cell lines and tissues, compared with matched non-tumor tissues and human endocervical epithelial cells. Also, miR-205 was inversely correlated with histological differentiation, metastasis, International Federation of Gynecology and Obstetrics stage, and the expression of insulin-like growth factor receptor 1 messenger RNA and protein. Besides, miR-205 or insulin-like growth factor receptor 1 expression is an independent prognostic factor. Mechanically, ectopic expression of miR-205 decreased proliferation, colony formation, and some proliferation/apoptosis-related proteins in cervical cancer cells. Ectopic expression of miR-205 caused G1 arrest. Luciferase reporter assays confirmed that binding of miR-205 to the 3′ untranslated region of insulin-like growth factor receptor 1 may pote...

https://journals.sagepub.com/doi/pdf/10.1177/1010428317701308

MiR-205 serves as a prognostic factor and suppresses proliferation and invasion by targeting insulin-like growth factor receptor 1 in human cervical cancer.

Distant metastasis is the predominant pattern of gastric cancer (GC) recurrence, and is the most common cause of cancer‑associated mortality. Accumulating evidence has suggested that aberrant activation of epithelial‑mesenchymal transition has a crucial role in the genesis, invasion and metastasis of various types of cancer, including GC. Using Cell Counting kit‑8 and Transwell assays, the effects of microRNA (miR)‑205 on the proliferation, migration and invasion of NCI‑H87 GC cells were determined, and the potential underlying mechanisms were explored. The results of the present study demonstrated that miR‑205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT. Upon transfection with miR‑205, the epithelial marker CDH1 (E‑cadherin) was upregulated, and the mesenchymal markers CDH2 (N‑cadherin) and vimentin were suppressed. Furthermore, zinc‑finger E‑box‑binding homeobox factor‑1 (ZEB1) was identified as a putative target gene of miR‑205 in GC, which may be associated with its suppressive effects. The results of the present study may provide novel diagnostic and therapeutic options for the treatment of human GC.

/pdf/microrna-205-suppresses-the-invasion-and-epithelial-2y9rewv64m.pdf

MicroRNA-205 suppresses the invasion and epithelial-mesenchymal transition of human gastric cancer cells

Objective The aim of this investigation was to study the effects of Runt-related transcription factor 2 (Runx2) on the junctional epithelium and alveolar bone. Methods The attachment level of the junctional epithelium and the resorption of alveolar bone were analyzed by histology and scanning electron microscopy. The expression of amelotin was determined by immunohistochemistry, Western blot, and real-time PCR. The ultrastructure of the dentogingival interface was observed by transmission electron microscopy. Results The cKO mice demonstrated remarkable attachment loss, epithelial hyperplasia, and alveolar bone loss. The relative protein and mRNA expression of amelotin was increased in the junctional epithelium of the cKO mice. The attachment apparatus of the cKO mice showed ultrastructural deficiency. Conclusions Loss of Runx2 led to the junctional epithelium and alveolar bone defects in mice. Runx2 may play a crucial role in maintaining the integrity of the dentogingival junction and the normal structure of alveolar bone.

Epithelium-Specific Runx2 knockout mice display junctional epithelium and alveolar bone defects

Amelotin (Amtn) is a recently identified enamel protein secreted by ameloblasts at late stage of enamel development. Runt‑related transcription factor 2 (Runx2) in combination with the coactivator core‑binding factor β (Cbfβ) regulates the early stages of tooth development. The aim of the present study was to investigate the role of Runx2 in the regulation of Amtn gene expression in ameloblasts. Immunohistochemistry was performed and the results revealed that Runx2 protein was predominantly expressed in the nuclei of ameloblasts during the transition stage and the maturation stage of enamel development, whereas Cbfβ was expressed in ameloblasts from the secretory stage to the maturation stage. Reverse transcription‑quantitative polymerase chain reaction results demonstrated that Runx2 knockdown decreased Amtn expression in ameloblast‑lineage cells and co‑expression of Runx2 and Cbfβ in ameloblast lineage cells induced an upregulation in Amtn gene expression. Two putative Runx2‑binding sites within the Amtn promoter were identified using bioinformatics analysis. Results of an electrophoretic mobility shift assay and chromatin immunoprecipitation indicated that Runx2/Cbfβ bound to specific DNA sequences. Site‑directed mutagenesis of the Runx2 binding sites within the Amtn promoter resulted in decreased basal promoter activity and did not affect the overexpressed Runx2/Cbfβ. The results of the present study suggest that Runx2 upregulates Amtn gene expression via binding directly to Runx2 sites within the Amtn promoter during amelogenesis.

/pdf/combination-of-runx2-and-cbfb-upregulates-amelotin-gene-3n2vzbv5pv.pdf

Combination of Runx2 and Cbfβ upregulates Amelotin gene expression in ameloblasts by directly interacting with cis‑enhancers during amelogenesis.

Efficacy of MR diffusion kurtosis imaging for differentiating low-grade from high-grade glioma before surgery: A systematic review and meta-analysis

The "Hand as Foot" teaching method in the trachea anatomy.

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