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long non-coding rna LINC01194 promotes the inflammatory response and apoptosis of lipopolysaccharide-treated MLE-12 cells through the miR-203a-3p/MIP-2 axis

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CANADIAN JOUrnaL OF PHYSIOLOGY AND PHARMACOLOGY 2022年第5期100卷 402-411页

作者： Shen, Yuyao Zhao, Senwei Hua, Minglei Qingdao Univ Dept Resp Med Affiliated Yantai Yuhuangding Hosp Shandong 264000 Peoples R China Linyi Peoples Hosp Dept EICU Linyi 276000 Shandong Peoples R China Zaozhuang Municipal Hosp Dept Resp Med Xincheng Branch Zaozhuang 277000 Shandong Peoples R China

Acute lung injury (ALI) induced by bacteria lipopolysaccharide (LPS) is characterized by the upregulation of the apoptosis rate of tissue cells and aggravation of inflammatory response. Although many studies have focused on the pathogenesis of this disease, its mechanism remains unknown. This study examined the regulatory role of long non-coding rna (lncrna) LINC01194 in the progression of ALI through various bioinforrnatics analyses and experimental work, including ELISA assay, dual-luciferase reporter assay, biotinylated rna pull-down assay, and Western blot analysis. The result showed that the LINC01194 was overexpressed in the ALI-induced mice model. We observed a significant upregulation of LINC01194 in LPS-treated mouse lung epithelial type II cells (MLE-12 cells) after 24 h of induction. Bioinformatics analysis, ELISA assay, quantitative reverse transcription polymerase chain reaction analysis, biotinylated rna pull-down assay, apoptosis test, and Western blot analysis demonstrated that the LINC01194 could act as a microrna (miR) miR-203a-3p sponge to activate the inflammatory response in LPS-induced ALI model through post-transcriptional upregulation of macrophage inflammatory protein (MIP-2). We showed that LINC01194 regulates the inflammatory response and apoptosis of LPS-induced mice and MLE-12 cells via the miR-203a-3p/MIP-2 axis. LINC01194 could be a potential biomarker for early diagnosis and the treatment of ALI.

关键词： acute lung injury long non-coding rna TNF-alpha MIP-2

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long non-coding rna-small nucleolar rna host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microrna-449a/TNF-α-induced protein 3-interacting protein 2 axis

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BIOENGINEERED 2022年第4期13卷 10215-10226页

作者： He, Chunlei Xiao, Jianhua Ye, Yongjun Huang, Shiqiao Zhong, Yanchun Liu, Lulin Liu, Wuyang Liu, Sheng Gannan Med Univ Dept Orthoped Affiliated Hosp 1 128 Jinling Rd Ganzhou 341000 Jiangxi Peoples R China

The current study aimed to explore the anti-inflammatory effects of long non-coding rna-small nucleolar rna host gene 7 (lncrna-SNHG7) and its mechanism in spinal cord injury (SCI) models. SCI models were established both in vivo and in vitro. Reverse transcription-quantitative PCR was performed to determine the expression levels of Incrna-SNHG7 in SCI models. Bioinformatics analysis and dual-luciferase reporter assays were carried out to confirm the interaction between Incrna-SNHG7 with microrna (miR)-499a and TNF-alpha-induced protein 3-interacting protein 2 (TNIP2). In addition, cell viability, apoptosis, and the secretion of inflammatory cytokines were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometric analysis, and enzyme linked immunosorbent assay (ELISA), respectively. The results showed that lncrna-SNHG7 was markedly downregulated in the SCI model group. Lncrna-SNHG7 directly bound to miR-499a, which in turn directly targeted TNIP2. In addition, TNIP2 was significantly decreased in SCI rats and lipopolysaccharide (LPS)-treated PC-12 cells. The in vitro results in PC-12 cells revealed that Incrna-SNHG7 overexpression attenuated neuronal cell death and SCI-mediated inflammatory responses by regulating miR-449a expression. Furthermore, miR-499a knockdown inhibited LPS-induced PC-12 cell injury by targeting TNIP2. In conclusion, Incrna-SNHG7 modulates the apoptosis and inflammation of PC-12 cells by regulating the miR-449a/TNIP2/NF-kappa B signaling pathway. [GRAPHICS] .

关键词： Spinal cord injury microrna long non-coding rna TNF-alpha-induced protein 3-interacting protein 2 NF-kappa B pathway

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long non-coding rna PCAT19 safeguards DNA in quiescent endothelial cells by preventing uncontrolled phosphorylation of RPA2

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CELL REPORTS 2022年第7期41卷 000-000页

作者： Oo, James A. Palfi, Katalin Warwick, Timothy Wittig, Ilka Prieto-Garcia, Cristian Matkovic, Vigor Tomaskovic, Ines Boos, Frederike Ponce, Judit Izquierdo Teichmann, Tom Petriukov, Kirill Haydar, Shaza Maegdefessel, Lars Wu, Zhiyuan Minh Duc Pham Krishnan, Jaya Baker, Andrew H. Guenther, Stefan Ulrich, Helle D. Dikic, Ivan Leisegang, Matthias S. Brandes, Ralf P. Goethe Univ Inst Cardiovasc Physiol Theodor Stern Kai 7 D-60596 Frankfurt Germany Max Planck Inst Heart & Lung Res D-61231 Bad Nauheim Germany Goethe Univ Fac Med Inst Biochem 2 D-60596 Frankfurt Germany Inst Mol Biol IMB D-55128 Mainz Germany Univ Edinburgh Ctr Cardiovasc Sci Queens Med Res Inst Edinburgh EH16 4TJ Midlothian Scotland German Ctr Cardiovasc Res DZHK Partner Site RheinMain Frankfurt Germany Goethe Univ Inst Cardiovasc Physiol Funct Prote D-60596 Frankfurt Germany Tech Univ Munich Dept Vasc & Endovasc Surg Klinikum Rechts Isar D-81675 Munich Germany Goethe Univ Ctr Mol Med Inst Cardiovasc Regenerat D-60596 Frankfurt Germany German Ctr Cardiovasc Res DZHK Partner Site Munich Munich Germany Genome Biol Theodor Stern Kai 7 D-60596 Frankfurt Germany Cardio Pulm Inst Giessen Germany Univ Maastricht CARIM Inst Univ Single 50 NL-6200 Maastricht Netherlands Goethe Univ Buchmann Inst Mol Life Sci D-60438 Frankfurt Germany Max Planck Inst Biophys Max Von Laue Str 3 D-60438 Frankfurt Germany

In healthy vessels, endothelial cells maintain a stable, differentiated, and growth-arrested phenotype for years. Upon injury, a rapid phenotypic switch facilitates proliferation to restore tissue perfusion. Here we report the identification of the endothelial cell-enriched long non-coding rna (lncrna) PCAT19, which con-tributes to the proliferative switch and acts as a safeguard for the endothelial genome. PCAT19 is enriched in confluent, quiescent endothelial cells and binds to the full replication protein A (RPA) complex in a DNA dam- age-and cell-cycle-related manner. Our results suggest that PCAT19 limits the phosphorylation of RPA2, pri-marily on the serine 33 (S33) residue, and thereby facilitates an appropriate DNA damage response while slowing cell cycle progression. Reduction in PCAT19 levels in response to either loss of cell contacts or knockdown promotes endothelial proliferation and angiogenesis. Collectively, PCAT19 acts as a dynamic guardian of the endothelial genome and facilitates rapid switching from quiescence to proliferation.

关键词： long non-coding rna endothelial cells replication protein A quiescence checkpoint control ataxia telangiectasia and Rad3 related cell cycle PCAT19 DNA damage

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The clinical value of serum long non-coding rna human leukocyte antigen complex group 11/microrna-532-3p in the diagnosis and prognosis of patients with acute myocardial infarction undergoing percutaneous coronary intervention

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JOUrnaL OF CARDIOTHORACIC SURGERY 2024年第1期19卷 555页

作者： Cao, Yu Yu, Gaixia Bai, Jing Gansu Med Coll Affiliated Hosp Dept Cardiovasc Med 296 Kongtong East Rd Pingliang 744000 Gansu Peoples R China Gansu Med Coll Dept Children Care Affiliated Hosp Pingliang 744000 Peoples R China

BackgroundAcute myocardial infarction (AMI) is a cardiovascular disease with the highest morbidity and mortality rate in the world. Several studies have suggested that abnormal regulation of non-coding rnas (ncrnas) may play a vital role in the occurrence and progress of *** purpose of this study was to investigate the clinical values of human leukocyte antigen complex group 11 (HCG11) or miR-532-3p in the diagnosis and prognosis of patients with AMI after percutaneous coronary intervention (PCI).MethodsThe clinical data of 100 AMI patients who underwent PCI were analyzed retrospectively. According to whether major adverse cardiovascular events (MACE) occurred after PCI, they were divided into MACE group (n = 38) and non-MACE group (n = 62). Basic clinical data and serum HCG11 and miR-532-3p levels were analyzed. Multivariate Cox regression analysis was performed to evaluate the risk factors for MACE, and the receiver operator characteristic (ROC) curve was constructed to assess the clinical predictive value of HCG11 and miR-532-3p for *** with the control group, the serum HCG11 level and miR-532-3p in AMI patients were significantly increased or decreased, and the serum levels of HCG11 and miR-532-3p in the MACE group were significantly increased and decreased, compared with those in non-MACE group. Multivariate Cox regression showed that HCG11 and miR-532-3p were risk factors for MACE occurrence. ROC curve investigated that HCG11 combined with miR-532-3p has accurate predictive value for *** study showed that serum HCG11 and miR-532-3p have certain predictive value for MACE after PCI in patients with AMI. The serum levels of HCG11 and miR-532-3p in patients with AMI were significantly higher and lower than those in control group, *** with the MACE group, the levels of HCG11 and miR-532-3p in the non-MACE group showed an increasing and decreasing *** regression analysis showed that high

关键词： Acute myocardial infarction long non-coding rna Microrna Percutaneous coronary intervention Major adverse cardiovascular events Prognosis

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Research Progress of long non-coding rna-ZFAS1 in Malignant Tumors

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CELL BIOCHEMISTRY AND BIOPHYSICS 2024年第4期82卷 3145-3156页

作者： Liu, Xin Ma, Zhong Zhang, Xianxu Li, Shicheng An, Jiangdong Luo, Zhiqiang Lanzhou Univ Hosp 2 Dept Orthopaed Lanzhou 730030 Gansu Peoples R China Key Lab Bone & Joint Dis Res Gansu Prov Lanzhou 730030 Gansu Peoples R China

long non-coding rnas (lncrnas), although incapable of encoding proteins, play crucial roles in multiple layers of gene expression regulation, epigenetic modifications, and post-transcriptional regulation. Zinc finger antisense 1 (ZFAS1), a lncrna located in the 20q13 region of the human genome, exhibits dual functions as an oncogene or tumor suppressor in various human malignancies. ZFAS1 plays a crucial role in cancer progression, metastasis, invasion, apoptosis, cell cycle regulation, and drug resistance through complex molecular mechanisms. Additionally, ZFAS1 has a long half-life of over 16 h, demonstrating exceptional stability, and making it a potential biomarker. This review integrates recent studies on the role and molecular mechanisms of ZFAS1 in malignancies and summarizes its clinical significance. By summarizing the role of ZFAS1 in cancer, we aim to highlight its potential as an anti-cancer biomarker and therapeutic target.

关键词： long non-coding rna ZFAS1 Malignant tumors Molecular mechanism

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Transcription of the Antisense long non-coding rna, SUPPRESSOR OF FEMINIZATION, Represses Expression of the Female-Promoting Gene FEMALE GAMETOPHYTE MYB in the Liverwort Marchantia polymorpha

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PLANT AND CELL PHYSIOLOGY 2024年第3期65卷 338-349页

作者： Kajiwara, Tomoaki Miyazaki, Motoki Yamaoka, Shohei Yoshitake, Yoshihiro Yasui, Yukiko Nishihama, Ryuichi Kohchi, Takayuki Kyoto Univ Grad Sch Biostudies Kitashirakawa Oiwake ChoSakyo Ku Kyoto 6068502 Japan Tokyo Univ Sci Fac Sci & Technol Dept Appl Biol Sci 2641 YamazakiNoda Chiba 2788510 Japan

Sexual differentiation is a fundamental process in the life cycles of land plants, ensuring successful sexual reproduction and thereby contributing to species diversity and survival. In the dioicous liverwort Marchantia polymorpha, this process is governed by an autosomal sex-differentiation locus comprising FEMALE GAMETOPHYTE MYB (FGMYB), a female-promoting gene, and SUPPRESSOR OF FEMINIZATION (SUF), an antisense strand-encoded long non-coding rna (lncrna). SUF is specifically transcribed in male plants and suppresses the expression of FGMYB, leading to male differentiation. However, the molecular mechanisms underlying this process remain elusive. Here, we show that SUF acts through its transcription to suppress FGMYB expression. Transgene complementation analysis using CRISPR/Cas9D10A-based large-deletion mutants identified a genomic region sufficient for the sex differentiation switch function in the FGMYB-SUF locus. Inserting a transcriptional terminator sequence into the SUF-transcribed region resulted in the loss of SUF function and allowed expression of FGMYB in genetically male plants, leading to conversion of the sex phenotype from male to female. Partial deletions of SUF had no obvious impact on its function. Replacement of the FGMYB sequence with that of an unrelated gene did not affect the ability of SUF transcription to suppress sense-strand expression. Taken together, our findings suggest that the process of SUF transcription, rather than the resulting transcripts, is required for controlling sex differentiation in M. polymorpha.

关键词： Antisense transcription long non-coding rna Marchantia polymorpha Reproduction Sex differentiation

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Common variation in a long non-coding rna gene modulates variation of circulating TGF-β2 levels in metastatic colorectal cancer patients (Alliance)

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BMC GENOMICS 2024年第1期25卷 1页

作者： Quintanilha, Julia C. F. Sibley, Alexander B. Liu, Yingmiao Niedzwiecki, Donna Halabi, Susan Rogers, Layne O'Neil, Bert Kindler, Hedy Kelly, William Venook, Alan McLeod, Howard L. Ratain, Mark J. Nixon, Andrew B. Innocenti, Federico Owzar, Kouros Univ North Carolina Chapel Hill UNC Eshelman Sch Pharm Chapel Hill NC USA Duke Univ Med Ctr Duke Canc Inst Durham NC 27710 USA Duke Univ Med Ctr Dept Med Durham NC USA Duke Univ Sch Med Dept Biostat & Bioinformat Durham NC 27710 USA Duke Univ Alliance Stat & Data Management Ctr Durham NC 27708 USA Indiana Univ Melvin & Bren Simon Canc Ctr Indianapolis IN USA Univ Chicago Dept Med Chicago IL USA Thomas Jefferson Univ Sidney Kimmel Canc Ctr Dept Med Oncol Philadelphia PA USA Univ Calif San Francisco Dept Med San Francisco CA USA Univ North Carolina Chapel Hill Chapel Hill NC USA Utah Tech Univ St George UT USA Univ North Carolina Chapel Hill Sch Pharm Chapel Hill NC USA

Background Herein, we report results from a genome-wide study conducted to identify protein quantitative trait loci (pQTL) for circulating angiogenic and inflammatory protein markers in patients with metastatic colorectal cancer (mCRC). The study was conducted using genotype, protein marker, and baseline clinical and demographic data from CALGB/SWOG 80405 (Alliance), a randomized phase III study designed to assess outcomes of adding VEGF or EGFR inhibitors to systemic chemotherapy in mCRC patients. Germline DNA derived from blood was genotyped on whole-genome array platforms. The abundance of protein markers was quantified using a multiplex enzyme-linked immunosorbent assay from plasma derived from peripheral venous blood collected at baseline. A robust rank-based method was used to assess the statistical significance of each variant and protein pair against a strict genome-wide level. A given pQTL was tested for validation in two external datasets of prostate (CALGB 90401) and pancreatic cancer (CALGB 80303) patients. Bioinformatics analyses were conducted to further establish biological bases for these findings. Results The final analysis was carried out based on data from 540,021 common typed genetic variants and 23 protein markers from 869 genetically estimated European patients with mCRC. Correcting for multiple testing, the analysis discovered a novel cis-pQTL in LINC02869, a long non-coding rna gene, for circulating TGF-beta 2 levels (rs11118119;AAF = 0.11;P-value < 1.4e-14). This finding was validated in a cohort of 538 prostate cancer patients from CALGB 90401 (AAF = 0.10, P-value < 3.3e-25). The analysis also validated a cis-pQTL we had previously reported for VEGF-A in advanced pancreatic cancer, and additionally identified trans-pQTLs for VEGF-R3, and cis-pQTLs for CD73. Conclusions This study has provided evidence of a novel cis germline genetic variant that regulates circulating TGF-beta 2 levels in plasma of patients with advanced mCRC and prostate ca

关键词： Cancer Common germline variation Genome-wide analysis study Circulating protein biomarkers Protein quantitative trait loci Inflammatory markers Angiogenesis markers TGF-beta 2 long non-coding rna

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long non-coding rna signatures and related signaling pathway in T-cell acute lymphoblastic leukemia

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CLINICAL & TRANSLATIONAL ONCOLOGY 2022年第11期24卷 2081-2089页

作者： Yousefi, Homayon Purrahman, Daryush Jamshidi, Mohammad Lak, Elena Keikhaei, Bijan Mahmoudian-Sani, Mohammad-Reza Ahvaz Jundishapur Univ Med Sci Hlth Res Inst Thalassemia & Hemoglobinopathy Res Ctr Ahvaz Iran Lorestan Univ Med Sci Razi Herbal Med Res Ctr Khorramabad Iran Ahvaz Jundishapur Univ Med Sci Sch Med Dept Internal Med Ahvaz Iran

T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy caused by clonal proliferation of T-cell pre-cursors arising from the thymus. Although the optimized chemotherapy regimen could improve the outcome of such patients, some challenges such as higher risk for induction failure, early relapse and isolated central nervous system (CNS) relapse occurring in T-ALL patients are of great significance, leading to increased mortality rates. long non-coding rna (lncrna) is a key component involved in cell signaling through a variety of mechanisms in regulating gene expression. Oncogenes and tumor suppressors are no exception and their expression can be affected by lncrnas. In addition, accumulating researches in samples from T-ALL patients as well as pre-clinical studies in mice suggest that the expression profile of lncrnas in T-ALL could be aberrant, resulting in deregulation of target genes and downstream signaling pathways. In addition, accumulating researches in samples from T-ALL patients as well as pre-clinical studies in mice suggest that the expression profile of lncrnas in T-ALL could be aberrant, resulting in deregulation of target genes and downstream signaling pathways. These lncrnas may be determinants of proliferation, apoptosis, and drug resistance observed in T-ALL. Thus, lncrnas can be a good tool to develop novel strategies against cancer cells in the treatment of relapsed and refractory T-ALL. They can also act as promoting biomarkers in assessing T-ALL and differentiating between patients with poor prognosis and good prognosis.

关键词： T-acute lymphoblastic leukemia long non-coding rna Signaling pathway Drug resistance Prognostic

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Advancements in long non-coding rna-based therapies for cancer: targeting, delivery, and clinical implications

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MEDICAL ONCOLOGY 2024年第11期41卷 292页

作者： Ammad, Muhammad Javed, Zeeshan Sadia, Haleema Ahmed, Rais Akbar, Ali Nadeem, Tariq Calina, Daniela Sharifi-Rad, Javad Univ Karachi Dept Biotechnol Karachi Pakistan Univ Punjab Ctr Appl Mol Biol Lahore Pakistan BUITEMS Dept Biotechnol Quetta Pakistan Cholistan Univ Veterniary & Anim Sci Bahawalpur Dept Microbiol Bahawalpur Pakistan Univ Swat Ctr Biotechnol & Microbiol Swat Pakistan Univ Punjab Ctr Excellence Mol Biol Lahore Pakistan Univ Med & Pharm Craiova Dept Clin Pharm Craiova 200349 Romania Univ Espiritu Santo Samborondon 092301 Ecuador Univ Golfo Ctr Estudios Tecnol Veracruz Mexico Korea Univ Coll Med Dept Med Seoul 02841 South Korea

long non-coding rnas (lncrnas) have been in the spotlight for the past two decades due to their extensive role in regulating a wide range of cellular processes. Development, differentiation, regulation, and modulation are some of the vital cellular cascades coordinated by these molecules. Despite their importance, there has been limited literature on their practical implications in cancer prevention. Advancements in lncrna biology have enabled the characterization of numerous secondary structures and sequence motifs, which could serve as potential targets for cellular therapies. Several studies have highlighted the involvement of lncrnas in human pathologies, where they can be targeted by small molecules or antisense oligonucleotides to prevent diseases. However, progress has been hindered by the challenge of developing specific delivery vehicles for targeted delivery. Recent improvements in sequence optimization and nucleotide modification have enhanced drug stability and reduced the immunogenicity of lncrna-based therapies, yet further advances are needed to fully realize their potential in treating complex diseases like cancer. This review aims to explore current lncrna biology, their mechanisms of action, nanoformulation strategies, and the clinical trials focused on lncrna delivery systems.

关键词： long non-coding rna Cancer Therapeutics Nano-delivery Clinical trials

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A long non-coding rna lnc210 promotes adipogenic differentiation of buffalo intramuscular adipocytes

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ANIMAL BIOTECHNOLOGY 2023年第7期34卷 2736-2744页

作者： Zhu, Ruirui Guo, Duo Li, Ruirui Feng, Ye Yang, Xintong Huang, Qixin Zheng, Yuanyu Shi, Deshun Huang, Jieping Guangxi Univ State Key Lab Conservat & Utilizat Subtrop Agrobi Nanning 530005 Guangxi Peoples R China

Intramuscular fat (IMF) content is one of the most significant factors influencing beef quality in terms of tenderness, flavor, and juiciness. Thus, internal factors affecting IMF deposition have received considerable attention for decades. In this study, we demonstrated a long non-coding rna, lnc210, promoted adipogenic differentiation of buffalo intramuscular adipocytes. lnc210 was rich in adipose tissue and showed increased expression with the adipogenic differentiation of buffalo intramuscular adipocytes. lnc210 was mainly expressed in the nucleus of adipocytes. Full-length lnc210 was obtained by rapid amplification of cDNA ends technology. lnc210 overexpression promoted lipid accumulation by upregulating the mrna expression of peroxisome proliferator-activated receptor gamma (PPARG) and CCAAT enhancer binding protein alpha (C/EBP alpha) in buffalo intramuscular adipocytes. These results provide a basis for an in-depth analysis of the role of lnc210 in accelerating IMF deposition in buffaloes.

关键词： Bubalus bubalis long non-coding rna intramuscular adipocytes adipogenic differentiation expression

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