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Alteration in the expression of microrna-21 regulated target genes:Role in breast cancer

BIOCELL 2022年第2期46卷 309-324页

作者： PRIYANKA THAKUR REENA V.SAINI ANIL K.CHHILLAR NEERAJ K.SAINI VIJAY KUMAR THAKUR SAMARJEET SINGH SIWAL ADESH K.SAINI Faculty of Sciences Shoolini UniversitySolan173229India Department of Biotechnology MMECMaharishi Markandeshwar(Deemed to be University)Ambala133207India Maharishi Markandeshwar University Solan173229India Centre of Biotechnology Maharshi Dayanand UniversityRohtak124001India School of Biotechnology Jawaharlal Nehu UniversityNew Delhi110067India Biorefining and Advanced Materials Research Center Scotland’s Rural College(SRUC)EdinburghEH93JGUK Department of Chemistry MMECMaharishi Markandeshwar(Deemed to be University)Ambala133207India

Breast cancer,also recognized as the principal cause of cancer-related deaths among women,is the second most familiar and prevalent form of *** diagnostic and prognostic biomarkers that are highly specific are urgently needed for its early ***(mirnas),a class of non-coding rnas,are known to control the biological processes involving transcription,post-transcriptional and covalent modifications,splicing,translation,cell differentiation,proliferation,apoptosis,cancer progression,and *** dysregulation in mirna expression,demonstrating their oncogenic and tumor-suppressive functions,contributes to cancer ***-21(miR-21),an‘onco-miR’in breast cancer,is involved in tumor progression and metastasis by suppressing the activity of the target gene via its interaction with the 3’UTR of the target *** upregulation of miR-21 is observed in many instances of breast *** review aims to summarize the current understanding of miR-21 in the regulation of important cellular functions via regulation of its target *** discuss its biosynthesis,oncogenic function in breast cancer,and different methods used for its *** will increase the current understanding of the role of miR-21 in breast cancer tumorigenesis,which will offer a perception of using miR-21 as an early detection molecular prognostic and diagnostic biomarker and as a therapeutic target in breast cancer care.

关键词： non-coding rna micrornas Breast cancer Tumor suppression Biomarker

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The human vault rna enhances tumorigenesis and chemoresistance through the lysosome in hepatocellular carcinoma

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AUTOPHAGY 2022年第1期18卷 191-203页

作者： Ferro, Iolanda Gavini, Jacopo Gallo, Stefano Bracher, Lisamaria Landolfo, Marc Candinas, Daniel Stroka, Deborah M. Polacek, Norbert Univ Bern Dept Chem Biochem & Pharmaceut Sci Freiestr 3 CH-3012 Bern Switzerland Bern Univ Hosp Inselspital Dept BioMed Res Dept Visceral Surg & Med Bern Switzerland Univ Bern Bern Switzerland Univ Bern Grad Sch Cellular & Biomed Sci Bern Switzerland

The small non-coding VTrna1-1 (vault rna 1-1) is known to confer resistance to apoptosis in several malignant cell lines and to also modulate the macroautophagic/autophagic flux in hepatocytes, thus highlighting its pro-survival role. Here we describe a new function of VTrna1-1 in regulating in vitro and in vivo tumor cell proliferation, tumorigenesis and chemoresistance. Knockout (KO) of VTrna1-1 in human hepatocellular carcinoma cells reduced nuclear localization of TFEB (transcription factor EB), leading to a downregulation of the coordinated lysosomal expression and regulation (CLEAR) network genes and lysosomal compartment dysfunction. We demonstrate further that impaired lysosome function due to loss of VTrna1-1 potentiates the anticancer effect of conventional chemotherapeutic drugs. Finally, loss of VTrna1-1 reduced drug lysosomotropism allowing higher intracellular compound availability and thereby significantly reducing tumor cell proliferation in vitro and in vivo. These findings reveal a so far unknown role of VTrna1-1 in the intracellular catabolic compartment and describe its contribution to lysosome-mediated chemotherapy resistance.

关键词： Chemoresistance lysosome non-coding rna tumorigenesis vault rna vtrna1-1

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Micropeptide MIAC inhibits the tumor progression by interacting with AQP2 and inhibiting EREG/EGFR signaling in renal cell carcinoma

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MOLECULAR CANCER 2022年第1期21卷 1-15页

作者： Li, Mengwei Liu, Guangxiang Jin, Xinrong Guo, Hongqian Setrerrahmane, Sarra Xu, Xindi Li, Tiantian Lin, Yunfei Xu, Hanmei China Pharmaceut Univ Engn Res Ctr Synthet Peptide Drug Discovery & Eva Nanjing 210009 Peoples R China China Pharmaceut Univ Minist Educ State Key Lab Nat Med Nanjing 210009 Peoples R China Nanjing Univ Drum Tower Hospita Med Sch 3 Depa Rtment Urol Nanjing 210008 Peoples R China NANJING ANJI Biotechnol CO LTD Nanjing 210033 Peoples R China

Background Although, micropeptides encoded by non-coding rna have been shown to have an important role in a variety of tumors processes, there have been no reports on micropeptide in renal cell carcinoma (RCC). Based on the micropeptide MIAC (micropeptide inhibiting actin cytoskeleton) discovered and named in the previous work, this study screened its tumor spectrum, and explored its mechanism of action and potential diagnosis and treatment value in the occurrence and development of renal carcinoma. Methods The clinical significance of MIAC in RCC was explored by bioinformatics analysis through high-throughput rna-seq data from 530 patients with kidney renal clear cell carcinoma (KIRC) in the TCGA database, and the detection of clinical samples of 70 cases of kidney cancer. In vitro and in vivo experiments to determine the role of MIAC in renal carcinoma cell growth and metastasis;High-throughput transcriptomics, western blotting, immunoprecipitation, molecular docking, affinity experiments, and Streptavidin pulldown experiments identify MIAC direct binding protein and key regulatory pathways. Results The analysis of 600 renal carcinoma samples from different sources revealed that the expression level of MIAC is significantly decreased, and corelated with the prognosis and clinical stage of tumors in patients with renal carcinoma. Overexpression of MIAC in renal carcinoma cells can significantly inhibit the proliferation and migration ability, promote apoptosis of renal carcinoma cells, and affect the distribution of cells at various stages. After knocking down MIAC, the trend is reversed. In vivo experiments have found that MIAC overexpression inhibit the growth and metastasis of RCC, while the synthetized MIAC peptides can significantly inhibit the occurrence and development of RCC in vitro and in vivo. Further mechanistic studies have demonstrated that MIAC directly bind to AQP2 protein, inhibit EREG/EGFR expression and activate downstream pathways PI3K/AKT and M

关键词： non-coding rna Micropeptides Renal cell carcinoma MIAC Aquaporin 2 EREG EGFR pathway

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Treatment of Intervertebral Disc Degeneration

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ORTHOPAEDIC SURGERY 2022年第7期14卷 1271-1280页

作者： Xin, Jingguo Wang, Yongjie Zheng, Zhi Wang, Shuo Na, Shibo Zhang, Shaokun First Hosp Jilin Univ Dept Spinal Surg 1 Xinmin St Changchun 130021 Peoples R China Jilin Engn Res Ctr Spine & Spinal Cord Injury Changchun Peoples R China Second Hosp Jilin Univ Dept Ophthalmol Changchun Peoples R China

Intervertebral disc degeneration (IDD) causes a variety of signs and symptoms, such as low back pain (LBP), intervertebral disc herniation, and spinal stenosis, which contribute to high social and economic costs. IDD results from many factors, including genetic factors, aging, mechanical injury, malnutrition, and so on. The pathological changes of IDD are mainly composed of the senescence and apoptosis of nucleus pulposus cells (NPCs), the progressive degeneration of extracellular matrix (ECM), the fibrosis of annulus fibrosus (AF), and the inflammatory response. At present, IDD can be treated by conservative treatment and surgical treatment based on patients' symptoms. However, all of these can only release the pain but cannot reverse IDD and reconstruct the mechanical function of the spine. The latest research is moving towards the field of biotherapy. Mesenchymal stem cells (MSCs) are regard as the potential therapy of IDD because of their ability to self-renew and differentiate into a variety of tissues. Moreover, the non-coding rnas (ncrnas) are found to regulate many vital processes in IDD. There have been many successes in the in vitro and animal studies of using biotherapy to treat IDD, but how to transform the experimental data to real therapy which can apply to humans is still a challenge. This article mainly reviews the treatment strategies and research progress of IDD and indicates that there are many problems that need to be solved if the new biotherapy is to be applied to clinical treatment of IDD. This will provide reference and guidance for clinical treatment and research direction of IDD.

关键词： Conservative treatment Intervertebral disc degeneration Mesenchymal stem cells non-coding rna Surgical treatment

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Evaluating changes in the expression of BCL-2 gene, lncrna SRA, and miR-361-3p in unexplained recurrent pregnancy loss

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NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS 2022年第9期41卷 891-899页

作者： Abbaskhani, Haleh Seifati, Seyed Morteza Salmani, Tayyebali Vojdani, Samaneh Al-Rubaye, Saja Yaseen, Rusul Hajiesmaeili, Yasaman Ghaderian, Sayyed Mohammad Hossein Islamic Azad Univ Ashkezar Branch Biol Dept Med Biotechnol Res Ctr Ashkezar Yazd Iran Shahid Beheshti Univ Med Sci Sch Med Dept Med Genet Tehran *** Iran York Univ Fac Hlth Toronto ON Canada Shahid Beheshti Univ Med Sci Urogenital Stem Cell Res Ctr Tehran Iran

Unexplained recurrent pregnancy loss (RPL) composed almost half of all diagnosed miscarriage cases. As the apoptosis pathway is involved in the pregnancy process the present investigation aimed to assess the differential expression of the BCL-2 gene, SRA lncrna, miR-361-3p in unexplained RPL patients. In this study, rna was isolated from 50 blood samples of people with a history of RPL, and 50 blood samples of people with healthy fertility. After cDNA synthesis from these samples, alterations in the expression levels of the above-mentioned genes were examined by Real-Time PCR. Our results showed that the expression of BCL-2 and lncrna SRA was significantly higher in the blood samples of RPL patients than in controls, while the expression of miR-361-3p was significantly downregulated. Besides, there were significant correlations between the changes in the expression of lncrna SRA and miR-361-3p with BCL-2, in positive and negative directions, respectively. Also, miR-361-3p presented as a good diagnostic marker with the highest AUC value to discriminate between RPL and the healthy control subjects. These results proposed that ncrnas may have a significant role in the regulation of apoptosis relates genes expression in RPL.

关键词： Apoptosis expression analysis non-coding rna recurrent pregnancy loss BCL-2 miR-361-3p

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The multifaceted actions of the lncrna H19 in cardiovascular biology and diseases

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CLINICAL SCIENCE 2022年第15期136卷 1157-1178页

作者： Busscher, Denise Boon, Reinier A. Juni, Rio P. Vrije Univ Amsterdam Dept Physiol Amsterdam UMC Boelelaan 1117 Amsterdam Netherlands Amsterdam Cardiovasc Sci Microcirculat Amsterdam Netherlands Goethe Univ Frankfurt Main Inst Cardiovasc Regenerat Ctr Mol Med Frankfurt Germany German Ctr Cardiovasc Res DZHK Partner site Frankfurt Rhein Main Frankfurt Germany

Cardiovascular diseases are the leading cause of death and debility worldwide. Various molecular mechanisms have been studied to better understand the development and progression of cardiovascular pathologies with hope to eradicate these diseases. With the advancement of the sequencing technology, it is revealed that the majority of our genome is non-coding. A growing body of literature demonstrates the critical role of long non-coding rnas (lncrnas) as epigenetic regulators of gene expression. Lncrnas can regulate cellular biological processes through various distinct molecular mechanisms. The abundance of lncrnas in the cardiovascular system indicates their significance in cardiovascular physiology and pathology. Lncrna H19, in particular, is a highly evolutionarily conserved lncrna that is enriched in cardiac and vascular tissue, underlining its importance in maintaining homeostasis of the cardiovascular system. In this review, we discuss the versatile function of H19 in various types of cardiovascular diseases. We highlight the current literature on H19 in the cardiovascular system and demonstrate how dysregulation of H19 induces the development of cardiovascular pathophysiology.

关键词： cardiovascular disease cardiovascular physiology large intervening non-coding rna lncrna H19 non-coding rna

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Microrna-378a-3p prevents initiation and growth of colorectal cancer by fine tuning polyamine synthesis

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CELL AND BIOSCIENCE 2022年第1期12卷 1-15页

作者： Liu, Ningning Zhang, Tianpeng Steer, Clifford J. Song, Guisheng Univ Minnesota Dept Med Minneapolis MN 55455 USA Univ Minnesota Dept Genet Cell Biol & Dev Minneapolis MN 55455 USA Univ Minnesota Div Gastroenterol Hepatol & Nutr 516 Delaware St SE Minneapolis MN 55455 USA

Background Inhibitors of ornithine decarboxylase (ODC) are effective at preventing colorectal cancer (CRC). However, their high toxicity limits their clinical application. This study was aimed to explore the potential of micrornas (mirnas) as an inhibitor of ODC. Methods mirna array was used to identify dysregulated mirnas in CRC tumors of mice and patients. Azoxymethane (AOM)/Dextran Sodium Sulfate (DSS) were used to induce CRC in mice. mirna function in carcinogenesis was determined by soft-agar colony formation, flow cytometry, and wound healing of CRC cells. Mini-circle was used to deliver mirna into colons. Results Mirna profiling identified miR-378a-3p (miR-378a) as the most reduced mirna in CRC tumors of patients and mice treated with AOM/DSS. Pathway array analysis revealed that miR-378a impaired c-MYC and ODC1 pathways. Further studies identified FOXQ1 (forkhead box Q1) and ODC1 as two direct targets of miR-378a. FOXQ1 activated transcription of c-MYC, a transcription activator of ODC1. In addition to directly targeting ODC1, miR-378a also inhibited expression of ODC1 via the FOXQ1-cMYC axis, thereby inhibiting polyamine synthesis in human CRC cells. Phenotypically, by reducing polyamine synthesis, miR-378a induced apoptosis and inhibited proliferation and migration of CRC cells, while disrupting the association of miR-378a with FOXQ1 and ODC1 offset the effects of miR-378a, suggesting that FOXQ1 and ODC1 were required for miR-378a to inhibit CRC cell growth. MiR-378a treatment robustly prevented growth of HCC by inhibiting polyamine synthesis in AOM/DSS mice. Conclusion MiR-378a prevents CRC by inhibiting polyamine synthesis, suggesting its use as a novel ODC inhibitor against CRC.

关键词： Ornithine decarboxylase inhibitor c-Myc signaling non-coding rna

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Challenges in defining the functional, non-coding, expressed genome of members of the Mycobacterium tuberculosis complex

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MOLECULAR MICROBIOLOGY 2022年第1期117卷 20-31页

作者： Stiens, Jennifer Arnvig, Kristine B. Kendall, Sharon L. Nobeli, Irene Birkbeck Univ London Inst Struct & Mol Biol Biol Sci Malet St London WC1E 7HX England UCL Inst Struct & Mol Biol Div Biosci London England Royal Vet Coll Ctr Emerging Endem & Exot Dis Pathobiol & Populat Hatfield Herts England

A definitive transcriptome atlas for the non-coding expressed elements of the members of the Mycobacterium tuberculosis complex (MTBC) does not exist. Incomplete lists of non-coding transcripts can be obtained for some of the reference genomes (e.g., M. tuberculosis H37Rv) but to what extent these transcripts have homologues in closely related species or even strains is not clear. This has implications for the analysis of transcriptomic data;non-coding parts of the transcriptome are often ignored in the absence of formal, reliable annotation. Here, we review the state of our knowledge of non-coding rnas in pathogenic mycobacteria, emphasizing the disparities in the information included in commonly used databases. We then proceed to review ways of combining computational solutions for predicting the non-coding transcriptome with experiments that can help refine and confirm these predictions.

关键词： mycobacteria Mycobacterium tuberculosis non-coding rna rna-seq transcriptome

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New insights into epigenetic regulation of resistance to PD-1/PD-L1 blockade cancer immunotherapy: mechanisms and therapeutic opportunities (vol 11, 101, 2022)

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EXPERIMENTAL HEMATOLOGY & ONCOLOGY 2022年第1期11卷 1-10页

作者： Dai, Mengyuan Liu, Miao Yang, Hua Kuecuek, Can You, Hua Chongqing Med Univ Pediat Res Inst Natl Clin Res Ctr Child Hlth & Disorders Dept Hematol & OncolChildrens HospLab Excellence 136 Zhongshan Second Rd Chongqing 401122 Peoples R China Harvard Med Sch Brigham & Womens Hosp Dept Pathol Boston MA USA Foshan Univ Sch Med Dept Basic Med & Biomed Engn Foshan Peoples R China Dokuz Eylul Univ Izmir Int Biomed & Genome Inst Izmir Turkey Izmir Biomed & Genome Ctr Basic & Translat Res Program Izmir Turkey Dokuz Eylul Univ Fac Med Dept Med Biol Izmir Turkey

Programmed cell death protein 1(PD-1) is a type of immune-inhibitory checkpoint protein, which delivers inhibitory signals to cytotoxic T cells by binding to the programmed death ligand-1 (PD-L1) displayed on the surface of cancer cells. Antibodies blocking PD-1/PD-L1 interaction have been extensively used in treatment of human malignancies and have achieved promising outcomes in recent years. However, gradual development of resistance to PD-1/PD-L1 blockade has decreased the effectiveness of this immunotherapy in cancer patients. The underlying epigenetic mechanisms need to be elucidated for application of novel strategies overcoming this immunotherapy resistance. Epigenetic aberrations contribute to cancerogenesis by promoting different hallmarks of cancer. Moreover, these alterations may lead to therapy resistance, thereby leading to poor prognosis. Recently, the epigenetic regulatory drugs have been shown to decrease the resistance to PD-1/PD-L1 inhibitors in certain cancer patients. Inhibitors of the non-coding rnas, DNA methyltransferases, and histone deacetylases combined with PD-1/PD-L1 inhibitors have shown considerable therapeutic efficacy against carcinomas as well as blood cancers. Importantly, DNA methylation-mediated epigenetic silencing can inhibit antigen processing and presentation, which promotes cancerogenesis and aggravates resistance to PD-1/PD-L1 blockade immunotherapy. These observations altogether suggest that the combination of the epigenetic regulatory drugs with PD-1/PD-L1 inhibitors may present potential solution to the resistance caused by monotherapy with PD-1/PD-L1 inhibitors.

关键词： PD-1/PD-L1 Immune checkpoints Therapy resistance Epigenetic regulation DNA methyltransferase Histone deacetylase non-coding rna

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Application of epigenetics in dermatological research and skin management

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JOUrnaL OF COSMETIC DERMATOLOGY 2022年第5期21卷 1920-1930页

作者： He, Jianbiao He, Huaming Qi, Yufeng Yang, Jie Zhi, Leilei Jia, Yan Beijing Technol & Business Univ Coll Chem & Mat Engn Beijing Key Lab Plant Resources Res & Dev Beijing 100048 Peoples R China Beijing Technol & Business Univ Coll Chem & Mat Engn Key Lab Cosmet China Natl Light Ind Beijing Peoples R China Shandong Huawutang Biol Technol Co Ltd Shandong Peoples R China

Background Epigenetics has recently evolved from a collection of diverse phenomena to a defined and far-reaching field of study. Epigenetic modifications of the genome, such as DNA methylation and histone modifications, have been reported to play a role in some skin diseases or cancer. Aims The purpose of this article was to review the development of epigenetic in recent decades and their applications in dermatological research. Methods An extensive literature search was conducted on epigenetic modifications since the first research on epigenetic. Results This article summarizes the concept and development of epigenetics, as well as the process and principle of epigenetic modifications such as DNA methylation, histone modification, and non-coding rna. Their application in some skin diseases and cosmetic research and development is also summarized. Conclusions This information will help to understand the mechanisms of epigenetics and some non-coding rna, the discovery of the related drugs, and provide new insights for skin health management and cosmetic research and development.

关键词： dermatological research DNA methylation epigenetics histone modification non-coding rna

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