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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (12 October 2021) | Viewed by 33698

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Prof. Dr. Imad Kansau

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1. Faculté de Pharmacie, Université Paris-Saclay, 91400 Orsay, France
2. Hopital Antoine Beclere (APHP), 92140 Clamart, France
Interests: infectious diseases; microbiology; host-response; clostridioides difficile; inflammation cell signaling; flagella; TLR5 signaling; miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

An increasing interest in non-coding RNAs has developed in recent years. In particular, research on microRNAs, small natural sequences of 21 to 24 nucleotides, first identified in 1993, has made a leap forward with the identification of more than 2000 different miRNAs in humans, but also in animals and plants. Originating from the transcription of independent genes (canonical pathway) or introns of genes encoding proteins (alternative pathway) throughout genomes, these miRNAs are involved in a huge variety of biological processes including development, differentiation, response to stress, homeostasis, cell death, inflammation, and the host immune response. Moreover, a strong implication of miRNAs in a variety of human pathologies has been widely described in the literature. These small molecules have also aroused great interest because of their enormous therapeutic potential. In fact, their specific mechanism of action on target genes suggests their use as therapeutic candidates for human diseases through new approaches using nucleic acids. However, faced with these major challenges, it is important to fully understand the complex mechanisms of inhibition through partial complementarity of transcription of miRNAs as well as the specific cell signaling pathways specifically regulated by miRNAs in cell. This Special Issue will be dedicated to the role of miRNAs on cell physiology and human pathology. All studies which help to enrich knowledge on the intimate mechanisms of gene regulation exerted by miRNAs and signaling pathways involving miRNAs in different physiological and pathological situations will be welcome.

Prof. Dr. Imad Kansau
Guest Editor

Manuscript Submission Information

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Keywords

MicroRNAs
Inhibition of gene expression
MiRNA targets
Seed sequence
Cell signaling
Immune response
Innate immune response
TLR signaling pathways
Regulation of gene expression
MiRNA mimics
MiRNA antagonist

Related Special Issue

MicroRNA Signaling in Human Diseases 2.0 in International Journal of Molecular Sciences (16 articles)

Published Papers (11 papers)

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Research

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13 pages, 4103 KiB

Open AccessArticle

Dexamethasone Suppresses Palatal Cell Proliferation through miR-130a-3p

by Hiroki Yoshioka, Goo Jun, Akiko Suzuki and Junichi Iwata

Int. J. Mol. Sci. 2021, 22(22), 12453; https://doi.org/10.3390/ijms222212453 - 18 Nov 2021

Cited by 6 | Viewed by 2349

Abstract

Cleft lip with or without cleft palate (CL/P) is one of the most common congenital birth defects. This study aims to identify novel pathogenic microRNAs associated with cleft palate (CP). Through data analyses of miRNA-sequencing for developing palatal shelves of C57BL/6J mice, we found that miR-449a-3p, miR-449a-5p, miR-449b, miR-449c-3p, and miR-449c-5p were significantly upregulated, and that miR-19a-3p, miR-130a-3p, miR-301a-3p, and miR-486b-5p were significantly downregulated, at embryonic day E14.5 compared to E13.5. Among them, overexpression of the miR-449 family (miR-449a-3p, miR-449a-5p, miR-449b, miR-449c-3p, and miR-449c-5p) and miR-486b-5p resulted in reduced cell proliferation in primary mouse embryonic palatal mesenchymal (MEPM) cells and mouse cranial neural crest cell line O9-1. On the other hand, inhibitors of miR-130a-3p and miR-301a-3p significantly reduced cell proliferation in MEPM and O9-1 cells. Notably, we found that treatment with dexamethasone, a glucocorticoid known to induce CP in mice, suppressed miR-130a-3p expression in both MEPM and O9-1 cells. Moreover, a miR-130a-3p mimic could ameliorate the cell proliferation defect induced by dexamethasone through normalization of Slc24a2 expression. Taken together, our results suggest that miR-130-3p plays a crucial role in dexamethasone-induced CP in mice. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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14 pages, 3660 KiB

Open AccessCommunication

Targeting the Highly Expressed microRNA miR-146b with CRISPR/Cas9n Gene Editing System in Thyroid Cancer

by Daniel Casartelli de Santa-Inez, Cesar Seigi Fuziwara, Kelly Cristina Saito and Edna Teruko Kimura

Int. J. Mol. Sci. 2021, 22(15), 7992; https://doi.org/10.3390/ijms22157992 - 27 Jul 2021

Cited by 11 | Viewed by 3261

Abstract

Thyroid cancer is the most common endocrine malignancy, and the characterization of the genetic alterations in coding-genes that drive thyroid cancer are well consolidated in MAPK signaling. In the context of non-coding RNAs, microRNAs (miRNAs) are small non-coding RNAs that, when deregulated, cooperate to promote tumorigenesis by targeting mRNAs, many of which are proto-oncogenes and tumor suppressors. In thyroid cancer, miR-146b-5p is the most overexpressed miRNA associated with tumor aggressiveness and progression, while the antisense blocking of miR-146b-5p results in anti-tumoral effect. Therefore, inactivating miR-146b has been considered as a promising strategy in thyroid cancer therapy. Here, we applied the CRISPR/Cas9n editing system to target the MIR146B gene in an aggressive anaplastic thyroid cancer (ATC) cell line. For that, we designed two single-guide RNAs cloned into plasmids to direct Cas9 nickase (Cas9n) to the genomic region of the pre-mir-146b structure to target miR-146b-5p and miR-146b-3p sequences. In this plasmidial strategy, we cotransfected pSp-Cas9n-miR-146b-GuideA-puromycin and pSp-Cas9n-miR-146b-GuideB-GFP plasmids in KTC2 cells and selected the puromycin resistant + GFP positive clones (KTC2-Cl). As a result, we observed that the ATC cell line KTC2-Cl1 showed a 60% decrease in the expression of miR-146b-5p compared to the control, also showing reduced cell viability, migration, colony formation, and blockage of tumor development in immunocompromised mice. The analysis of the MIR146B edited sequence shows a 5 nt deletion in the miR-146b-5p region and a 1 nt deletion in the miR-146b-3p region in KTC2-Cl1. Thus, we developed an effective CRISPR/Cas9n system to edit the MIR146B miRNA gene and reduce miR-146b-5p expression which constitutes a potential molecular tool for the investigation of miRNAs function in thyroid cancer. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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13 pages, 1744 KiB

Open AccessArticle

miR-373-3p Regulates Invasion and Migration Abilities of Trophoblast Cells via Targeted CD44 and Radixin

by Hyun-Jung Lee, Seung Mook Lim, Hee Yeon Jang, Young Ran Kim, Joon-Seok Hong and Gi Jin Kim

Int. J. Mol. Sci. 2021, 22(12), 6260; https://doi.org/10.3390/ijms22126260 - 10 Jun 2021

Cited by 9 | Viewed by 2345

Abstract

Preterm labor (PTL) is one of the obstetric complications, and is known to be associated with abnormal maternal inflammatory response and intrauterine inflammation and/or infection. However, the expression of specific miRNAs associated with PTL is not clear. In this study, we performed combination analysis of miRNA array and gene array, and then selected one miRNA (miR-373-3p) and its putative target genes (CD44 and RDX) that exhibited large expression differences in term and PTL placentas with or without inflammation. Using qRT-PCR and luciferase assays, we confirmed that miR-373-3p directly targeted CD44 and RDX. Overexpression of miR-373-3p reduced the migration and invasion of trophoblast cells, while inhibition of miR-373-3p restored the migration and invasion abilities of trophoblast cells. Finally, we validated the expression of miR-373-3p and its target genes in clinical patients’ blood. miR-373-3p was increased in PTL patients’ blood, and was the most expressed in PTL patients’ blood with inflammation. In addition, by targeting the miR-373-3p, CD44 and RDX was decreased in PTL patients’ blood, and their expression were the lowest in PTL patients’ blood with inflammation. Taken together, these findings suggest that miR-373-3p and its target genes can be potential biomarkers for diagnosis of PTL. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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12 pages, 1047 KiB

Open AccessArticle

Mirna Expression in Glaucomatous and TGFβ2 Treated Lamina Cribrosa Cells

by Navita N. Lopez, Rajiv Rangan, Abbot F. Clark and Tara Tovar-Vidales

Int. J. Mol. Sci. 2021, 22(12), 6178; https://doi.org/10.3390/ijms22126178 - 8 Jun 2021

Cited by 3 | Viewed by 2266

Abstract

Glaucoma is a group of optic neuropathies that leads to irreversible vision loss. The optic nerve head (ONH) is the site of initial optic nerve damage in glaucoma. ONH-derived lamina cribrosa (LC) cells synthesize extracellular matrix (ECM) proteins; however, these cells are adversely affected in glaucoma and cause detrimental changes to the ONH. LC cells respond to mechanical strain by increasing the profibrotic cytokine transforming growth factor-beta 2 (TGFβ2) and ECM proteins. Moreover, microRNAs (miRNAs or miR) regulate ECM gene expression in different fibrotic diseases, including glaucoma. A delicate homeostatic balance between profibrotic and anti-fibrotic miRNAs may contribute to the remodeling of ONH. This study aimed to determine whether modulation of miRNAs alters the expression of ECM in human LC cells. Primary human normal and glaucoma LC cells were grown to confluency and treated with or without TGFβ2 for 24 h. Differences in expression of miRNAs were analyzed using miRNA qPCR arrays. miRNA PCR arrays showed that the miR-29 family was significantly decreased in glaucomatous LC cell strains compared to age-matched controls. TGFβ2 treatment downregulated the expression of multiple miRNAs, including miR-29c-3p, compared to controls in LC cells. LC cells transfected with miR-29c-3p mimics or inhibitors modulated collagen expression. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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19 pages, 4867 KiB

Open AccessArticle

MiR-15a-5p Confers Chemoresistance in Acute Myeloid Leukemia by Inhibiting Autophagy Induced by Daunorubicin

by Emeline Bollaert, Melissa Claus, Virginie Vandewalle, Sandrine Lenglez, Ahmed Essaghir, Jean-Baptiste Demoulin and Violaine Havelange

Int. J. Mol. Sci. 2021, 22(10), 5153; https://doi.org/10.3390/ijms22105153 - 13 May 2021

Cited by 15 | Viewed by 2491

Abstract

Anthracyclines remain a cornerstone of induction chemotherapy for acute myeloid leukemia (AML). Refractory or relapsed disease due to chemotherapy resistance is a major obstacle in AML management. MicroRNAs (miRNAs) have been observed to be involved in chemoresistance. We previously observed that miR-15a-5p was overexpressed in a subgroup of chemoresistant cytogenetically normal AML patients compared with chemosensitive patients treated with daunorubicin and cytarabine. MiR-15a-5p overexpression in AML cells reduced apoptosis induced by both drugs in vitro. This study aimed to elucidate the mechanisms by which miR-15a-5p contributes to daunorubicin resistance. We showed that daunorubicin induced autophagy in myeloid cell lines. The inhibition of autophagy reduced cell sensitivity to daunorubicin. The overexpression of miR-15a-5p decreased daunorubicin-induced autophagy. Conversely, the downregulation of miR-15a-5p increased daunorubicin-induced autophagy. We found that miR-15a-5p targeted four genes involved in autophagy, namely ATG9a, ATG14, GABARAPL1 and SMPD1. Daunorubicin increased the expression of these four genes, and miR-15a-5p counteracted this regulation. Inhibition experiments with the four target genes showed the functional effect of miR-15a-5p on autophagy. In summary, our results indicated that miR-15a-5p induces chemoresistance in AML cells through the abrogation of daunorubicin-induced autophagy, suggesting that miR-15a-5p could be a promising therapeutic target for chemoresistant AML patients. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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12 pages, 1416 KiB

Open AccessArticle

Phenytoin Inhibits Cell Proliferation through microRNA-196a-5p in Mouse Lip Mesenchymal Cells

by Hiroki Yoshioka, Sai Shankar Ramakrishnan, Akiko Suzuki and Junichi Iwata

Int. J. Mol. Sci. 2021, 22(4), 1746; https://doi.org/10.3390/ijms22041746 - 9 Feb 2021

Cited by 8 | Viewed by 2270

Abstract

Cleft lip (CL) is one of the most common birth defects. It is caused by either genetic mutations or environmental factors. Recent studies suggest that environmental factors influence the expression of noncoding RNAs [e.g., microRNA (miRNA)], which can regulate the expression of genes crucial for cellular functions. In this study, we examined which miRNAs are associated with CL. Among 10 candidate miRNAs (miR-98-3p, miR-101a-3p, miR-101b-3p, miR-141-3p, miR-144-3p, miR-181a-5p, miR-196a-5p, miR-196b-5p, miR-200a-3p, and miR-710) identified through our bioinformatic analysis of CL-associated genes, overexpression of miR-181a-5p, miR-196a-5p, miR-196b-5p, and miR-710 inhibited cell proliferation through suppression of genes associated with CL in cultured mouse embryonic lip mesenchymal cells (MELM cells) and O9-1 cells, a mouse cranial neural crest cell line. In addition, we found that phenytoin, an inducer of CL, decreased cell proliferation through miR-196a-5p induction. Notably, treatment with a specific inhibitor for miR-196a-5p restored cell proliferation through normalization of expression of CL-associated genes in the cells treated with phenytoin. Taken together, our results suggest that phenytoin induces CL through miR-196a-5p induction, which suppresses the expression of CL-associated genes. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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21 pages, 4897 KiB

Open AccessArticle

MiR-21 Is Required for the Epithelial–Mesenchymal Transition in MDA-MB-231 Breast Cancer Cells

by Elif Damla Arisan, Ozge Rencuzogullari, Clara Cieza-Borrella, Francesc Miralles Arenas, Miriam Dwek, Sigrun Lange and Pinar Uysal-Onganer

Int. J. Mol. Sci. 2021, 22(4), 1557; https://doi.org/10.3390/ijms22041557 - 4 Feb 2021

Cited by 31 | Viewed by 5373

Abstract

Breast cancer (BCa) is one of the leading health problems among women. Although significant achievements have led to advanced therapeutic success with targeted therapy options, more efforts are required for different subtypes of tumors and according to genomic, transcriptomic, and proteomic alterations. This study underlines the role of microRNA-21 (miR-21) in metastatic MDA-MB-231 breast cancer cells. Following the knockout of miR-21 from MDA-MB-231 cells, which have the highest miR-21 expression levels compared to MCF-7 and SK-BR-3 BCa cells, a decrease in epithelial-mesenchymal transition (EMT) via downregulation of mesenchymal markers was observed. Wnt-11 was a critical target for miR-21, and the Wnt-11 related signaling axis was altered in the stable miR-21 knockout cells. miR-21 expression was associated with a significant increase in mesenchymal markers in MDA-MB-231 BCa cells. Furthermore, the release of extracellular vesicles (EVs) was significantly reduced in the miR-21 KO cells, alongside a significant reduction in relative miR-21 export in EV cargo, compared with control cells. We conclude that miR-21 is a leading factor involved in mesenchymal transition in MDA-MB-231 BCa. Future therapeutic strategies could focus on its role in the treatment of metastatic breast cancer. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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19 pages, 2324 KiB

Open AccessArticle

LncRNA H19-Derived miR-675-5p Accelerates the Invasion of Extravillous Trophoblast Cells by Inhibiting GATA2 and Subsequently Activating Matrix Metalloproteinases

by Manabu Ogoyama, Akihide Ohkuchi, Hironori Takahashi, Dongwei Zhao, Shigeki Matsubara and Toshihiro Takizawa

Int. J. Mol. Sci. 2021, 22(3), 1237; https://doi.org/10.3390/ijms22031237 - 27 Jan 2021

Cited by 13 | Viewed by 2508

Abstract

The invasion of extravillous trophoblast (EVT) cells into the maternal decidua, which plays a crucial role in the establishment of a successful pregnancy, is highly orchestrated by a complex array of regulatory mechanisms. Non-coding RNAs (ncRNAs) that fine-tune gene expression at epigenetic, transcriptional, and post-transcriptional levels are involved in the regulatory mechanisms of EVT cell invasion. However, little is known about the characteristic features of EVT-associated ncRNAs. To elucidate the gene expression profiles of both coding and non-coding transcripts (i.e., mRNAs, long non-coding RNAs (lncRNAs), and microRNAs (miRNAs)) expressed in EVT cells, we performed RNA sequencing analysis of EVT cells isolated from first-trimester placentae. RNA sequencing analysis demonstrated that the lncRNA H19 and its derived miRNA miR-675-5p were enriched in EVT cells. Although miR-675-5p acts as a placental/trophoblast growth suppressor, there is little information on the involvement of miR-675-5p in trophoblast cell invasion. Next, we evaluated a possible role of miR-675-5p in EVT cell invasion using the EVT cell lines HTR-8/SVneo and HChEpC1b; overexpression of miR-675-5p significantly promoted the invasion of both EVT cell lines. The transcription factor gene GATA2 was shown to be a target of miR-675-5p; moreover, small interfering RNA-mediated GATA2 knockdown significantly promoted cell invasion. Furthermore, we identified MMP13 and MMP14 as downstream effectors of miR-675-5p/GATA2-dependent EVT cell invasion. These findings suggest that miR-675-5p-mediated GATA2 inhibition accelerates EVT cell invasion by upregulating matrix metalloproteinases. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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9 pages, 1416 KiB

Open AccessArticle

From miRNA Target Gene Network to miRNA Function: miR-375 Might Regulate Apoptosis and Actin Dynamics in the Heart Muscle via Rho-GTPases-Dependent Pathways

by German Osmak, Ivan Kiselev, Natalia Baulina and Olga Favorova

Int. J. Mol. Sci. 2020, 21(24), 9670; https://doi.org/10.3390/ijms21249670 - 18 Dec 2020

Cited by 7 | Viewed by 1712

Abstract

MicroRNAs (miRNAs) are short, single-stranded, non-coding ribonucleic acid (RNA) molecules, which are involved in the regulation of main biological processes, such as apoptosis or cell proliferation and differentiation, through sequence-specific interaction with target mRNAs. In this study, we propose a workflow for predicting miRNAs function by analyzing the structure of the network of their target genes. This workflow was applied to study the functional role of miR-375 in the heart muscle (myocardium), since this miRNA was previously shown to be associated with heart diseases, and data on its function in the myocardium are mostly unclear. We identified PIK3CA, RHOA, MAPK3, PAFAH1B1, CTNNB1, MYC, PRKCA, ERBB2, and CDC42 as key genes in the miR-375 regulated network and predicted the possible function of miR-375 in the heart muscle, consisting mainly in the regulation of the Rho-GTPases-dependent signaling pathways. We implemented our algorithm for miRNA function prediction into a Python module, which is available at GitHub. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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Review

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29 pages, 5084 KiB

Open AccessReview

The Expression of Non-Coding RNAs and Their Target Molecules in Rheumatoid Arthritis: A Molecular Basis for Rheumatoid Pathogenesis and Its Potential Clinical Applications

by Chang-Youh Tsai, Song-Chou Hsieh, Chih-Wei Liu, Cheng-Hsun Lu, Hsien-Tzung Liao, Ming-Han Chen, Ko-Jen Li, Cheng-Han Wu, Cheih-Yu Shen, Yu-Min Kuo and Chia-Li Yu

Int. J. Mol. Sci. 2021, 22(11), 5689; https://doi.org/10.3390/ijms22115689 - 26 May 2021

Cited by 16 | Viewed by 4130

Abstract

Rheumatoid arthritis (RA) is a typical autoimmune-mediated rheumatic disease presenting as a chronic synovitis in the joint. The chronic synovial inflammation is characterized by hyper-vascularity and extravasation of various immune-related cells to form lymphoid aggregates where an intimate cross-talk among innate and adaptive immune cells takes place. These interactions facilitate production of abundant proinflammatory cytokines, chemokines and growth factors for the proliferation/maturation/differentiation of B lymphocytes to become plasma cells. Finally, the autoantibodies against denatured immunoglobulin G (rheumatoid factors), EB virus nuclear antigens (EBNAs) and citrullinated protein (ACPAs) are produced to trigger the development of RA. Furthermore, it is documented that gene mutations, abnormal epigenetic regulation of peptidylarginine deiminase genes 2 and 4 (PADI2 and PADI4), and thereby the induced autoantibodies against PAD2 and PAD4 are implicated in ACPA production in RA patients. The aberrant expressions of non-coding RNAs (ncRNAs) including microRNAs (miRs) and long non-coding RNAs (lncRNAs) in the immune system undoubtedly derange the mRNA expressions of cytokines/chemokines/growth factors. In the present review, we will discuss in detail the expression of these ncRNAs and their target molecules participating in developing RA, and the potential biomarkers for the disease, its diagnosis, cardiovascular complications and therapeutic response. Finally, we propose some prospective investigations for unraveling the conundrums of rheumatoid pathogenesis. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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32 pages, 2013 KiB

Open AccessReview

MicroRNAs as Modulators of Oral Tumorigenesis—A Focused Review

by Kumar Rishabh, Soham Khadilkar, Aviral Kumar, Ishu Kalra, Alan Prem Kumar and Ajaikumar B. Kunnumakkara

Int. J. Mol. Sci. 2021, 22(5), 2561; https://doi.org/10.3390/ijms22052561 - 4 Mar 2021

Cited by 44 | Viewed by 3882

Abstract

Oral cancers constitute the majority of head and neck tumors, with a relatively high incidence and poor survival rate in developing countries. While the five-year survival rates of the oral cancer patients have increased to 65%, the overall survival for advanced stages has been at 27% for the past ten years, emphasizing the necessity for further understanding the etiology of the disease, diagnosis, and formulating possible novel treatment regimens. MicroRNAs (miRNAs), a family of small non-coding RNA, have emerged as master modulators of gene expression in various cellular and biological process. Aberrant expression of these dynamic molecules has been associated with many human diseases, including oral cancers. The deregulated miRNAs have been shown to control various oncogenic processes, including sustaining proliferative signaling, evading growth suppressors, resisting cell death activating invasion and metastasis, and inducing angiogenesis. Hence, the aberrant expression of miRNAs associated with oral cancers, makes them potential candidates for the investigation of functional markers, which will aid in the differential diagnosis, prognosis, and development of novel therapeutic regimens. This review presents a holistic insight into our understanding of the role of miRNAs in regulating various hallmarks of oral tumorigenesis. Full article

(This article belongs to the Special Issue MicroRNA Signaling in Human Diseases)

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