Editorial

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Open AccessEditorial

MicroRNAs and Other Non-Coding RNAs as Regulators, Biomarkers, and Therapeutic Targets

by Wan Lee

Int. J. Mol. Sci. 2024, 25(7), 3998; https://doi.org/10.3390/ijms25073998 - 03 Apr 2024

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Over the past few decades, the field of RNA research in molecular and cellular biology has undergone a dramatic transformation [...] Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

Research

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16 pages, 2369 KiB

Open AccessArticle

Expression of Tumor Suppressor FHIT Is Regulated by the LINC00173-SNAIL Axis in Human Lung Adenocarcinoma

by Takahito Suzuki, Satoshi Sakai, Kosuke Ota, Mika Yoshida, Chiharu Uchida, Hiroyuki Niida, Takafumi Suda, Masatoshi Kitagawa and Tatsuya Ohhata

Int. J. Mol. Sci. 2023, 24(23), 17011; https://doi.org/10.3390/ijms242317011 - 30 Nov 2023

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Abstract

Long non-coding RNAs (lncRNAs) play a critical role in a variety of human diseases such as cancer. Here, to elucidate a novel function of a lncRNA called LINC00173, we investigated its binding partner, target gene, and its regulatory mechanism in lung adenocarcinoma, [...] Read more.

Long non-coding RNAs (lncRNAs) play a critical role in a variety of human diseases such as cancer. Here, to elucidate a novel function of a lncRNA called LINC00173, we investigated its binding partner, target gene, and its regulatory mechanism in lung adenocarcinoma, including the A549 cell line and patients. In the A549 cell line, RNA immunoprecipitation (RIP) assays revealed that LINC00173 efficiently binds to SNAIL. RNA-seq and RT-qPCR analyses revealed that the expression of FHIT was decreased upon LINC00173 depletion, indicating that FHIT is a target gene of LINC00173. Overexpression of SNAIL suppressed and depletion of SNAIL increased the expression of FHIT, indicating that SNAIL negatively regulates FHIT. The downregulation of FHIT expression upon LINC00173 depletion was restored by additional SNAIL depletion, revealing a LINC00173-SNAIL-FHIT axis for FHIT regulation. Data from 501 patients with lung adenocarcinoma also support the existence of a LINC00173-SNAIL-FHIT axis, as FHIT expression correlated positively with LINC00173 (p = 1.75 × 10⁻⁶) and negatively with SNAIL (p = 7.00 × 10⁻⁵). Taken together, we propose that LINC00173 positively regulates FHIT gene expression by binding to SNAIL and inhibiting its function in human lung adenocarcinoma. Thus, this study sheds light on the LINC00173-SNAIL-FHIT axis, which may be a key mechanism for carcinogenesis and progression in human lung adenocarcinoma. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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12 pages, 2586 KiB

Open AccessArticle

miR-136 Regulates the Proliferation and Adipogenic Differentiation of Adipose-Derived Stromal Vascular Fractions by Targeting HSD17B12

by Jianhua Liu, Yutong Che, Ke Cai, Bishi Zhao, Liying Qiao, Yangyang Pan, Kaijie Yang and Wenzhong Liu

Int. J. Mol. Sci. 2023, 24(19), 14892; https://doi.org/10.3390/ijms241914892 - 04 Oct 2023

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Abstract

Fat deposition involves the continuous differentiation of adipocytes and lipid accumulation. Studies have shown that microRNA miR-136 and 17β-hydroxysteroid dehydrogenase type 12 (HSD17B12) play important roles in lipid accumulation. However, the regulatory mechanism through which miR-136 targets HSD17B12 during ovine adipogenesis [...] Read more.

Fat deposition involves the continuous differentiation of adipocytes and lipid accumulation. Studies have shown that microRNA miR-136 and 17β-hydroxysteroid dehydrogenase type 12 (HSD17B12) play important roles in lipid accumulation. However, the regulatory mechanism through which miR-136 targets HSD17B12 during ovine adipogenesis remains unclear. This study aimed to elucidate the role of miR-136 and HSD17B12 in adipogenesis and their relationship in ovine adipose-derived stromal vascular fractions (SVFs). The target relationship between miR-136 and HSD17B12 was predicted and confirmed using bioinformatics and a dual-luciferase reporter assay. The results showed that miR-136 promoted proliferation and inhibited adipogenic differentiation of ovine SVFs. We also found that HSD17B12 inhibited proliferation and promoted adipogenic differentiation of ovine SVFs. Collectively, our results indicate that miR-136 facilitates proliferation and attenuates adipogenic differentiation of ovine SVFs by targeting HSD17B12. These findings provide a theoretical foundation for further elucidation of the regulatory mechanisms of lipid deposition in sheep. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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17 pages, 6257 KiB

Open AccessArticle

MicroRNA PC-3p-2869 Regulates Antler Growth and Inhibits Proliferation and Migration of Human Osteosarcoma and Chondrosarcoma Cells by Targeting CDK8, EEF1A1, and NTN1

by Fan Yang, Jin Wu, Mindie Zhao, Han Zheng, Jingyuan Suo, Xuedong Liu and Dong Zheng

Int. J. Mol. Sci. 2023, 24(13), 10840; https://doi.org/10.3390/ijms241310840 - 29 Jun 2023

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Abstract

MicroRNAs (miRNAs) play a crucial role in maintaining the balance between the rapid growth and suppression of tumorigenesis during antler regeneration. This study investigated the role of a novel miRNA, PC-3p-2869 (miR-PC-2869), in antler growth and its therapeutic potential in human osteosarcoma and [...] Read more.

MicroRNAs (miRNAs) play a crucial role in maintaining the balance between the rapid growth and suppression of tumorigenesis during antler regeneration. This study investigated the role of a novel miRNA, PC-3p-2869 (miR-PC-2869), in antler growth and its therapeutic potential in human osteosarcoma and chondrosarcoma. Stem-loop RT-qPCR showed that miR-PC-2869 was expressed extensively in diverse layers of antler tissues. Overexpression of miR-PC-2869 suppressed the proliferation and migration of antler cartilage cells. Similarly, heterologous expression of miR-PC-2869 reduced the proliferation, colony formation, and migration of osteosarcoma cell line MG63 and U2OS and chondrosarcoma cell line SW1353. Moreover, 18 functional target genes of miR-PC-2869 in humans were identified based on the screening of the reporter library. Among them, 15 target genes, including CDK8, EEF1A1, and NTN1, possess conserved miR-PC-2869-binding sites between humans and red deer (Cervus elaphus). In line with this, miR-PC-2869 overexpression decreased the expression levels of CDK8, EEF1A1, and NTN1 in MG63, SW1353, and antler cartilage cells. As expected, the knockdown of CDK8, EEF1A1, or NTN1 inhibited the proliferation and migration of MG63, SW1353, and antler cartilage cells, demonstrating similar suppressive effects as miR-PC-2869 overexpression. Furthermore, we observed that CDK8, EEF1A1, and NTN1 mediated the regulation of c-myc and cyclin D1 by miR-PC-2869 in MG63, SW1353, and antler cartilage cells. Overall, our work uncovered the cellular functions and underlying molecular mechanism of antler-derived miR-PC-2869, highlighting its potential as a therapeutic candidate for bone cancer. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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16 pages, 3681 KiB

Open AccessArticle

MicroRNA-146b-5p Suppresses Pro-Inflammatory Mediator Synthesis via Targeting TRAF6, IRAK1, and RELA in Lipopolysaccharide-Stimulated Human Dental Pulp Cells

by Peifeng Han, Keisuke Sunada-Nara, Nobuyuki Kawashima, Mayuko Fujii, Shihan Wang, Thoai Quoc Kieu, Ziniu Yu and Takashi Okiji

Int. J. Mol. Sci. 2023, 24(8), 7433; https://doi.org/10.3390/ijms24087433 - 18 Apr 2023

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Abstract

MicroRNA-146b-5p (miR-146b-5p) is up-regulated during and to suppress the inflammation process, although mechanisms involved in the action of miR-146b-5p have not been fully elucidated. This study examined the anti-inflammation effects of miR-146b-5p in lipopolysaccharide (LPS)-stimulated human dental pulp cells (hDPCs). An increase in [...] Read more.

MicroRNA-146b-5p (miR-146b-5p) is up-regulated during and to suppress the inflammation process, although mechanisms involved in the action of miR-146b-5p have not been fully elucidated. This study examined the anti-inflammation effects of miR-146b-5p in lipopolysaccharide (LPS)-stimulated human dental pulp cells (hDPCs). An increase in human miR-146b-5p (hsa-miR-146b-5p) expression following the mRNA expression of pro-inflammatory cytokines was observed in LPS-stimulated hDPCs. The expression of hsa-miR-146b-5p and pro-inflammatory cytokines was down-regulated by a nuclear factor-kappa B (NF-κB) inhibitor, and the expression of hsa-miR-146b-5p was also decreased by a JAK1/2 inhibitor. Enforced expression of hsa-miR-146b-5p abolished phosphorylation of NF-κB p65 and down-regulated the expression of pro-inflammatory cytokines and NF-κB signaling components, such as interleukin-1 receptor-associated kinase 1 (IRAK1), tumor necrosis factor receptor-associated factor 6 (TRAF6), and REL-associated protein involved in NF-κB (RELA). Expression of rat miR-146b-5p (rno-miR-146b-5p) and pro-inflammatory cytokine mRNA was also up-regulated in experimentally-induced rat pulpal inflammation in vivo, and rno-miR-146b-5p blocked the mRNA expression of pro-inflammatory mediators and NF-κB signaling components in LPS-stimulated ex vivo cultured rat incisor pulp tissues. These findings suggest that the synthesis of miR-146b-5p is controlled via an NF-κB/IL6/STAT3 signaling cascade, and in turn, miR-146b-5p down-regulates the expression of pro-inflammatory mediators by targeting TRAF6, IRAK1, and RELA in LPS-stimulated hDPCs. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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12 pages, 631 KiB

Open AccessArticle

The Expression Levels of MicroRNAs Differentially Expressed in Sudden Sensorineural Hearing Loss Patients’ Serum Are Unchanged for up to 12 Months after Hearing Loss Onset

by Reyhaneh Abgoon, Printha Wijesinghe, Cathie Garnis and Desmond A. Nunez

Int. J. Mol. Sci. 2023, 24(8), 7307; https://doi.org/10.3390/ijms24087307 - 15 Apr 2023

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Abstract

Sudden sensorineural hearing loss (SSNHL) is an acquired idiopathic hearing loss. Serum levels of small, non-coding RNAs and microRNAs (miRNAs) miR-195-5p/-132-3p/-30a-3p/-128-3p/-140-3p/-186-5p/-375-3p/-590-5p are differentially expressed in SSNHL patients within 28 days of hearing loss onset. This study determines if these changes persist by comparing [...] Read more.

Sudden sensorineural hearing loss (SSNHL) is an acquired idiopathic hearing loss. Serum levels of small, non-coding RNAs and microRNAs (miRNAs) miR-195-5p/-132-3p/-30a-3p/-128-3p/-140-3p/-186-5p/-375-3p/-590-5p are differentially expressed in SSNHL patients within 28 days of hearing loss onset. This study determines if these changes persist by comparing the serum miRNA expression profile of SSNHL patients within 1 month of hearing loss onset with that of patients 3–12 months after hearing loss onset. We collected serum from consenting adult SSNHL patients at presentation or during clinic follow-up. We matched patient samples drawn 3–12 months after hearing loss onset (delayed group, n = 9 patients) by age and sex to samples drawn from patients within 28 days of hearing loss onset (immediate group, n = 14 patients). We compared the real-time PCR-determined expression levels of the target miRNAs between the two groups. We calculated the air conduction pure-tone-averaged (PTA) audiometric thresholds in affected ears at the initial and final follow-up visits. We undertook inter-group comparisons of hearing outcome status and initial and final PTA audiometric thresholds. There was no significant inter-group difference in miRNA expression level, hearing recovery status and initial and final affected ear PTA audiometric thresholds. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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15 pages, 2868 KiB

Open AccessArticle

Mir-302a/TWF1 Axis Impairs the Myogenic Differentiation of Progenitor Cells through F-Actin-Mediated YAP1 Activation

by Mai Thi Nguyen and Wan Lee

Int. J. Mol. Sci. 2023, 24(7), 6341; https://doi.org/10.3390/ijms24076341 - 28 Mar 2023

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Abstract

Actin cytoskeleton dynamics have been found to regulate myogenesis in various progenitor cells, and twinfilin-1 (TWF1), an actin-depolymerizing factor, plays a vital role in actin dynamics and myoblast differentiation. Nevertheless, the molecular mechanisms underlying the epigenetic regulation and biological significance of TWF1 in [...] Read more.

Actin cytoskeleton dynamics have been found to regulate myogenesis in various progenitor cells, and twinfilin-1 (TWF1), an actin-depolymerizing factor, plays a vital role in actin dynamics and myoblast differentiation. Nevertheless, the molecular mechanisms underlying the epigenetic regulation and biological significance of TWF1 in obesity and muscle wasting have not been explored. Here, we investigated the roles of miR-302a in TWF1 expression, actin filament modulation, proliferation, and myogenic differentiation in C2C12 progenitor cells. Palmitic acid, the most prevalent saturated fatty acid (SFA) in the diet, decreased the expression of TWF1 and impeded myogenic differentiation while increasing the miR-302a levels in C2C12 myoblasts. Interestingly, miR-302a inhibited TWF1 expression directly by targeting its 3′UTR. Furthermore, ectopic expression of miR-302a promoted cell cycle progression and proliferation by increasing the filamentous actin (F-actin) accumulation, which facilitated the nuclear translocation of Yes-associated protein 1 (YAP1). Consequently, by suppressing the expressions of myogenic factors, i.e., MyoD, MyoG, and MyHC, miR-302a impaired myoblast differentiation. Hence, this study demonstrated that SFA-inducible miR-302a suppresses TWF1 expression epigenetically and impairs myogenic differentiation by facilitating myoblast proliferation via F-actin-mediated YAP1 activation. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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Review

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16 pages, 984 KiB

Open AccessReview

Tear Film MicroRNAs as Potential Biomarkers: A Review

by Jeremy Altman, Garrett Jones, Saleh Ahmed, Shruti Sharma and Ashok Sharma

Int. J. Mol. Sci. 2023, 24(4), 3694; https://doi.org/10.3390/ijms24043694 - 12 Feb 2023

Cited by 7 | Viewed by 3143

Abstract

MicroRNAs are non-coding RNAs that serve as regulatory molecules in a variety of pathways such as inflammation, metabolism, homeostasis, cell machinery, and development. With the progression of sequencing methods and modern bioinformatics tools, novel roles of microRNAs in regulatory mechanisms and pathophysiological states [...] Read more.

MicroRNAs are non-coding RNAs that serve as regulatory molecules in a variety of pathways such as inflammation, metabolism, homeostasis, cell machinery, and development. With the progression of sequencing methods and modern bioinformatics tools, novel roles of microRNAs in regulatory mechanisms and pathophysiological states continue to expand. Advances in detection methods have further enabled larger adoption of studies utilizing minimal sample volumes, allowing the analysis of microRNAs in low-volume biofluids, such as the aqueous humor and tear fluid. The reported abundance of extracellular microRNAs in these biofluids has prompted studies to explore their biomarker potential. This review compiles the current literature reporting microRNAs in human tear fluid and their association with ocular diseases including dry eye disease, Sjögren’s syndrome, keratitis, vernal keratoconjunctivitis, glaucoma, diabetic macular edema, and diabetic retinopathy, as well as non-ocular diseases, including Alzheimer’s and breast cancer. We also summarize the known roles of these microRNAs and shed light on the future progression of this field. Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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2 pages, 877 KiB

Open AccessCorrection

Correction: Han et al. MicroRNA-146b-5p Suppresses Pro-Inflammatory Mediator Synthesis via Targeting TRAF6, IRAK1, and RELA in Lipopolysaccharide-Stimulated Human Dental Pulp Cells. Int. J. Mol. Sci. 2023, 24, 7433

by Peifeng Han, Keisuke Sunada-Nara, Nobuyuki Kawashima, Mayuko Fujii, Shihan Wang, Thoai Quoc Kieu, Ziniu Yu and Takashi Okiji

Int. J. Mol. Sci. 2024, 25(4), 2049; https://doi.org/10.3390/ijms25042049 - 08 Feb 2024

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Abstract

In the original publication, there was a mistake in Figure 4J,K as published [...] Full article

(This article belongs to the Special Issue MicroRNAs and Other Non-coding RNAs as Regulators, Biomarkers, and Therapeutic Targets)

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