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.

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.

Objective: Gastric cancer (GC) is a common tumor malignancy with high incidence and poor prognosis. Radiotherapy is one of the main strategies for GC treatment, while development of radioresistance limits the effectiveness. microRNA-203 (miR-203) has been reported to participate in progression of GC, whereas its interaction with radiosensitivity of GC and the related mechanism remain largely unclear. Methods: The expressions of miR-203 and zinc finger E-box binding homeobox 1 (ZEB1) were measured in GC tissues and cells by quantitative real-time polymerase chain reaction or western blot. Survival fraction, cell viability and apoptosis were measured in GC cells after treatment of radiation by colony formation, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay or flow cytometry, respectively. Tumor volume and weight were detected in murine xenograft model after radiation treatment. The interaction between miR-203 and ZEB1 was explored by bioinformatics analysis and luciferase activity assay. Results: miR-203 expression was down-regulated and ZEB1 mRNA level was up-regulated in GC. The expression of miR-203 was associated with radiosensitivity of GC cells. Moreover, overexpression of miR-203 decreased survival fraction, cell viability and tumor growth but promoted cell apoptosis in radiation-treated GC cells. However, knockdown of miR-203 played an opposite effect. ZEB1 was validated as a target of miR-203, and it was involved in miR-203-mediated radiosensitivity of GC cells in vitro and in vivo. Conclusion: miR-203 promoted radiosensitivity of GC cells by targeting ZEB1, indicating miR-203 as a promising radiosensitizer for GC treatment.

/pdf/mir-203-acts-as-a-radiosensitizer-of-gastric-cancer-cells-by-3ji87adon5.pdf

MiR-203 acts as a radiosensitizer of gastric cancer cells by directly targeting ZEB1

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

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