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long noncoding rna ISA1 Protects Against Ischemic Brain Damage by Promoting the Transformation of Microglia Toward Anti-inflammatory Phenotype via the SOCS3/JAK2/STAT3 Pathway

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NEUROCHEMICAL RESEARCH 2025年第2期50卷 1-16页

作者： Lu, Ermei Zhou, Peng Li, Yuanyuan Chen, Jiale Zhang, Kexin Zhou, Kecheng Wenzhou Med Univ Wenzhou Cent Hosp Dingli Clin Coll Dept Pharm Wenzhou 325000 Zhejiang Peoples R China Wenzhou Med Univ Yuying Childrens Hosp Affliated Hosp 2 Rehabil Med Ctr Wenzhou Zhejiang Peoples R China Wenzhou Med Univ Sch Rehabil Med Wenzhou Zhejiang Peoples R China Wenzhou Med Univ Inst Neurosci Basic Med Coll Wenzhou Zhejiang Peoples R China

The shift of microglia towards an anti-inflammatory phenotype has been shown to decrease neuroinflammation, improve neurological function, and is considered a potential therapeutic approach for stroke. Abnormal expression of multiple long noncoding rna (Lncrna) has been discovered to be crucially related to the pathogenesis progress of ischemic brain injury. Here we concentrated on a novel Lncrna NR_037961.1, which we named ischemic stroke associated Lncrna1 (Lncrna ISA1). The expression of Lncrna ISA1 was notably decreased in brain tissue of middle cerebral artery occlusion (MCAO) mice. Overexpression of Lncrna ISA1 decreases cerebral infarction and brain edema, and improves cerebral blood flow and neurological outcome, promoting recovery of MCAO mice. Additionally, the neuroprotective effects that Lncrna ISA1 plays on MCAO mice are mediated by encouraging the transformation of microglia toward anti-inflammatory phenotype and alleviating neuroinflammation. Lncrna ISA1 facilitates the phenotypic transformation of microglia, closely linked to its promotion of SOCS3 expression and subsequent inhibition of the JAK2/STAT3 signaling pathway. Furthermore, downregulation of SOCS3 eliminated the effects of Lncrna ISA1 on transformation of microglia to anti-inflammatory phenotype. Our results indicate that Lncrna ISA1 promotes the anti-inflammatory polarization of microglia via regulation of the SOCS3/JAK2/STAT3 signaling pathway, and contributes to its neuroprotective effects in ischemic stroke.

关键词： Ischemic stroke Neuroinflammation long noncoding rna Microglia polarization SOCS3

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long noncoding rna semaphorin 6A-antisense rna 1 reduces hepatocellular carcinoma by promoting semaphorin 6A mrna degradation

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World Journal of Gastroenterology 2025年第13期31卷 138-151页

作者： Song-Man Yu Min Zhang Sha-Lin Li Si-Ya Pei Li Wu Xing-Wang Hu Yan-Kun Duan Department of Infectious Diseases Hunan Key Laboratory of Viral HepatitisXiangya HospitalCentral South UniversityChangsha 410008Hunan ProvinceChina Department of Blood Transfusion Xiangya HospitalCentral South UniversityChangsha 410008Hunan ProvinceChina Department of Infectious Diseases Hunan Key Laboratory of Viral HepatitisNational Clinical Research Center for Geriatric DisordersXiangya HospitalCentral South UniversityChangsha 410008Hunan ProvinceChina

BACKGROUND Hepatocellular carcinoma(HCC)is a prevalent malignant tumor with a poor prognosis,which is often associated with chronic hepatitis B virus infection in *** previous study has shown that long non-coding rna semaphorin 6Aantisense rna 1(SEMA6A-AS1)was significantly downregulated in hepatitis B virus-related HCC and associated with poor *** To explore the underlying mechanism of SEMA6A-AS1 in HCC *** The expression levels of SEMA6A-AS1 and SEMA6A were detected using quantitative polymerase chain reaction,immunohistochemistry and Western blot.A growth curve,colony formation,wound-healing and transwell(with or without Matrigel)assays were respectively performed to assess the proliferation,migration and invasion abilities of HCC *** cycle and apoptosis assays were performed by flow *** investigate the potential mechanism underpinning SEMA6A-AS1,we utilized tagged rna affinity purification,dual luciferase reporter assay and *** Downregulation of SEMA6A-AS1 in HCC was negatively correlated with SEMA6A protein ***6A was upregulated in HCC and correlated with high alpha-fetoprotein level,high Edmondson-Steiner grade and poor ***6A-AS1 significantly inhibited the proliferation,migration and invasion of HCC cells by combining with SEMA6A mrna and promoting its ***6A protein promoted the proliferation,migration and invasion of HCC cells by regulating the actin *** Our findings suggest that SEMA6A-AS1 can inhibit HCC progression through decreasing SEMA6A expression by promoting its mrna ***6A-AS1 may be a prognostic biomarker and therapeutic target for HCC.

关键词： long noncoding rna Semaphorin 6A antisense rna 1 Semaphorin 6A Hepatocellular carcinoma Liver cancer

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CASCADES, a novel SOX2 super-enhancer-associated long noncoding rna, regulates cancer stem cell specification and differentiation in glioblastoma

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MOLECULAR ONCOLOGY 2025年第3期19卷 764-784页

作者： Shahzad, Uswa Nikolopoulos, Marina Li, Christopher Johnston, Michael Wang, Jenny J. Sabha, Nesrin Varn, Frederick S. Riemenschneider, Alexandra Krumholtz, Stacey Krishnamurthy, Pranathi Meda Smith, Christian A. Karamchandani, Jason Watts, Jonathan K. Verhaak, Roel G. W. Gallo, Marco Rutka, James T. Das, Sunit Univ Toronto Inst Med Sci Fac Med Toronto ON Canada Hosp Sick Children Arthur & Sonia Labatt Brain Tumor Res Ctr Toronto ON Canada Univ Calgary Cumming Sch Med Dept Biochem & Mol Biol Charbonneau Canc InstAlberta Childrens Hosp Res I Calgary AB Canada Hosp Sick Children Program Genet & Genome Biol Toronto ON Canada Jackson Lab Genom Med Farmington CT USA Univ Massachusetts RNA Therapeut Inst Med Sch Worcester MA USA McGill Univ Hlth Ctr MUHC Montreal Neurol Inst Montreal PQ Canada Univ Toronto St Michaels Hosp Div Neurosurg Toronto ON M5B 1W8 Canada Univ Toronto Li Ka Shing Knowledge Inst Toronto ON M5B 1W8 Canada

Glioblastoma is the most common primary malignant brain tumor in adults, with a median survival of just over 1 year. The failure of available treatments to achieve remission in patients with glioblastoma (GBM) has been attributed to the presence of cancer stem cells (CSCs), which are thought to play a central role in tumor development and progression and serve as a treatment-resistant cell repository capable of driving tumor recurrence. In fact, the property of "stemness" itself may be responsible for treatment resistance. In this study, we identify a novel long noncoding rna (lncrna), cancer stem cell-associated distal enhancer of SOX2 (CASCADES), that functions as an epigenetic regulator in glioma CSCs (GSCs). CASCADES is expressed in isocitrate dehydrogenase (IDH)-wild-type GBM and is significantly enriched in GSCs. Knockdown of CASCADES in GSCs results in differentiation towards a neuronal lineage in a cell- and cancer-specific manner. Bioinformatics analysis reveals that CASCADES functions as a super-enhancer-associated lncrna epigenetic regulator of SOX2. Our findings identify CASCADES as a critical regulator of stemness in GSCs that represents a novel epigenetic and therapeutic target for disrupting the CSC compartment in glioblastoma.

关键词： cancer stem cells cell differentiation enhancers long noncoding rna SOX2 super-enhancers

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Investigator-initiated phase I trial of an oligonucleotide therapeutic targeting long noncoding rna TUG 1 for recurrent glioblastoma

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BMC CANCER 2025年第1期25卷 1-9页

作者： Deguchi, Shoichi Ohka, Fumiharu Shiba, Yoshiki Yamaguchi, Junya Sato, Aya Shinjo, Keiko Arakawa, Yoshiki Narita, Yoshitaka Kondo, Yutaka Saito, Ryuta Nagoya Univ Grad Sch Med Dept Neurosurg 65 Tsurumai ChoShowa Ku Nagoya Aichi 4668560 Japan Nagoya Univ Div Canc Biol Grad Sch Med Nagoya Japan Kyoto Univ Grad Sch Med Dept Neurosurg Kyoto Japan Natl Canc Ctr Dept Neurosurg & Neurooncol Tokyo Japan

BackgroundGlioblastoma (GB) is the most common and aggressive primary malignant brain tumor in adults. To date, no effective treatment has been reported for recurrent GB (rGB). long noncoding rna taurine upregulated gene 1 (TUG1), which is highly expressed in GB, resolves the formation of R-loops, thereby maintaining tumor growth. TUG1-targeting antisense oligonucleotide (ASO) (TUG1ASO) is a nucleotide therapeutic with drug delivery system that targets TUG1, demonstrating efficacy against GB in mouse models. This multicenter, first-in-human, phase I trial aims to investigate the safety and maximum tolerated dose (MTD) of *** study will enroll patients aged 18-75 years with rGB following postoperative temozolomide plus radiation therapy. The primary endpoints will be the safety and tolerability of TUG1ASO and the MTD. The secondary endpoints will be the response rate, duration of response, progression-free survival, overall survival, and pharmacokinetics of TUG1ASO. Dose escalation will be performed utilizing a 3 + 3 design with four dose levels. Unless the discontinuation criteria are met, four cycles will be administered, with each cycle lasting 7 days. Administration of TUG1ASO will be possible until the discontinuation criteria are ***1ASO is the first oligonucleotide therapeutic with drug delivery system targeting TUG1, expected to show an efficacy in rGB patients. In this first-in-human study, safety, tolerability and MTD of this new targeted therapy will be confirmed to find the recommended dose for the further clinical trial. This study may contribute to develop a new treatment option for rGB *** registrationJapan Registry of Clinical Trials (jRCT) 2041230136, registration date May 17, *** dateMay 17, *** datesJanuary 1, 2024, to present.

关键词： Recurrent glioblastoma TUG1 TUGIASO long noncoding rna

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Identification of a PANoptosis-related long noncoding rna risk signature for prognosis and immunology in colon adenocarcinoma

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BMC CANCER 2025年第1期25卷 1-21页

作者： Cui, Yuekai Mei, Jie Zhao, Shengsheng Zhu, Bingzi Lu, Jianhua Li, Hongzheng Bai, Binglong Sun, Weijian Jin, Wenyu Zhu, Xueqiong Rao, Shangrui Yi, Yongdong Wenzhou Med Univ Affiliated Hosp 2 Wenzhou Peoples R China Wenzhou Med Univ Yuying Childrens & Hosp Wenzhou Peoples R China Wenzhou Med Univ Affiliated Hosp 1 Wenzhou Peoples R China Wenzhou Med Univ Wenzhou Peoples R China

BackgroundPANoptosis, a complex programmed cell death (PCD) pathway that includes apoptosis, pyroptosis and necroptosis, is significantly involved in the progression of cancers. long noncoding rnas (lncrnas) play crucial roles in PCD. However, the predictive value of PANoptosis-related lncrnas (PRlncrnas) for colon adenocarcinoma (COAD) has not been *** expression data and clinical characteristics of patients with COAD were obtained from The Cancer Genome Atlas database. Differential expression analysis and Pearson correlation analysis were used to identify PRlncrnas. In addition to least absolute shrinkage and selection operator, univariate and multivariate Cox regression analyses were employed to obtain PRlncrnas for constructing a risk signature. Patients with COAD in the training set, testing set and entire set were stratified into high- and low-risk groups for further comparison of survival prognosis, using the median risk score as the cut-off point. Time-dependent receiver operating characteristic curves, a nomogram and multivariate Cox regression analysis were conducted to validate the risk signature in the testing set and the entire set. In addition, critical pathways, immune infiltration cells, immune checkpoint-related genes, Tumor Immune Dysfunction and Exclusion (TIDE) scores and antitumour drugs were compared between the two risk groups in the entire set. Correlations between ferroptosis, cuproptosis, disulfidptosis and the PRlncrna risk score were evaluated. Finally, a competitive endogenous rna (cerna) network was established, and enrichment analysis of the predicted mrnas was performed using Gene Ontology (GO) analysis. The Kaplan-Meier plotter database was used as an external database to confirm the accuracy of the risk signature in predicting patient prognosis. Additionally, small interfering rna (sirna), a cell counting kit- 8 assay, a cell colony formation assay, quantitative polymerase chain reaction (qPCR) and an apoptosis a

关键词： PANoptosis long noncoding rna Risk signature Colon adenocarcinoma

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DNA methylation of long noncoding rna cytochrome B in diabetic retinopathy

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NON-CODING rna RESEARCH 2025年 11卷 141-149页

作者： Kowluru, Renu A. Kumar, Jay Malaviya, Pooja Wayne State Univ Kresge Eye Inst Detroit MI 48202 USA

Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding rna (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (LncCytB), is also downregulated. This study aims to investigate the role of DNA methylation in the downregulation of LncCytB in diabetic retinopathy. Human retinal endothelial cells, incubated in 5 mM (normal) or 20 mM (high) D-glucose, in the presence/absence of Azacytidine (a DNA methyl transferase inhibitor) were analyzed for LncCytB DNA methylation by immunoprecipitation and methylation specific PCR techniques, and LncCytB transcripts by strand-specific PCR and rna-FISH. Mitochondrial genomic stability was evaluated by quantifying protective mtDNA nucleoids by SYBR green staining and by flow cytometry, and functional stability by oxygen consumption rate using Seahorse analyzer. Results were confirmed in an in vivo model using retina from diabetic rat. While high glucose elevated 5 mC and the ratio of methylated to unmethylated amplicons at LncCytB and down- regulated its transcripts, azacytidine prevented LncCytB DNA hypermethylation and decrease in its expression. Azacytidine also ameliorated decrease in nucleoids and oxygen consumption rate. Similarly, azacytidine prevented increase in retinal LncCytB DNA methylation and decrease in its expression in diabetic rats. Thus, DNA hypermethylation plays a major role in the downregulation of retinal LncCytB in diabetes, resulting in impaired mitochondrial homeostasis, and culminating in the development of diabetic retinopathy.

关键词： Diabetic retinopathy DNA methylation Epigenetics long noncoding rna Mitochondrial DNA

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long noncoding rna ZRANB2-AS2 promotes endothelial cell dysfunction by inhibiting phosphorylation of acetyl-CoA carboxylase 1 in diabetes

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Experimental Cell Research 2025年第2期448卷

作者： Chen, Tianchi Wang, Bing Li, Donglin Yu, Xinyu Lv, Kejia Zhu, Qianqian Qiu, Chenyang He, Yangyan Zhang, Hongkun Wu, Ziheng Department of Vascular Surgery The First Affiliated Hospital Zhejiang University School of Medicine Hangzhou China Zhejiang University School of Medicine Hangzhou China Department of Stomatology The First Affiliated Hospital Zhejiang University School of Medicine Hangzhou China

Lncrna has been implicated in the regulation of diabetes. We identified a novel lncrna that inhibits phosphorylation of acetyl-CoA carboxylase 1 to modulate the dysfunction of vascular endothelial cells under high glucose conditions. In vitro experiments were performed to investigate the effects of lnc rna ZRANB2-AS2 on ACC1 phosphorylation, free fatty acid and triglyceride levels, angiogenesis, cell apoptosis, cell proliferation and migration rate. Further, in vivo experiments were designed to examine the effects of lnc rna ZRANB2-AS2 on the level of ACC1, the limb ischemia and foot movement of mice, as well as on apoptosis, cell proliferation, and migration of vascular endothelial cells under conditions of high *** rna sequencing, we identified a lncrna, ZRANB2-AS2, which is highly expressed in human umbilical vein endothelial cells (HUVECs) under high glucose condition. We demonstrated that it could promote apoptosis and inhibit angiogenesis, proliferation and migration of endothelial cells. Using rna pull-down and RIP assays, the binding specificity of lncrna ZRANB2-AS2 and acetyl-CoA carboxylase 1(ACC1) was determined. We further established the rescue assay by adding CMS-121, a specific ACC1 inhibitor. These findings suggested that CMS-121 could reverse the inhibition of lncrna ZRANB2-AS2 on ACC1 phosphorylation, decrease intracellular free fatty acid and triglyceride levels. We conducted in vivo experiments to determine the inhibitory effect of lncrna ZRANB2-AS2 in diabetic mice model. Lnc ZRANB2-AS2 inhibits cell proliferation, migration and angiogenesis while accelerates apoptosis of endothelial cells by regulating the phosphorylation of acetyl-CoA carboxylase 1 in diabetes. © 2025

关键词： Cell dysfunction Diabetes long noncoding rna Vascular endothelial cell

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The Super Enhancer-Driven long noncoding rna PRKCQ-AS1 Promotes Neuroblastoma Tumorigenesis by Interacting With MSI2 Protein and Is Targetable by Small Molecule Compounds

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ADVANCED SCIENCE 2025年第0期 e2412520页

作者： Mondal, Sujanna Liu, Pei Y. Seneviratne, Janith De Weck, Antoine Venkat, Pooja Mayoh, Chelsea Wu, Jing Maag, Jesper Chen, Jingwei Wong, Matthew Bartonicek, Nenad Khoo, Poh Jin, Lei Ludlow, Louise E. Ziegler, David S. Trahair, Toby Mestdagh, Pieter Cheung, Belamy B. Li, Jinyan Dinger, Marcel E. Street, Ian Zhang, Xu D. Marshall, Glenn M. Liu, Tao Univ New South Wales Childrens Canc Inst Australia Sydney NSW 2052 Australia Univ New South Wales UNSW Ctr Childhood Canc Res Sydney NSW 2052 Australia Garvan Inst Med Res Genome Informat Genom & Epigenet Div 384 Victoria St Darlinghurst NSW 2010 Australia Univ Newcastle Sch Med & Publ Hlth Callaghan NSW 2308 Australia Zhengzhou Univ Henan Prov Peoples Hosp Translat Res Inst Tianjian Lab Adv Biomed SciAcad Med Sci Zhengzhou Peoples R China Univ Melbourne Royal Childrens Hosp Murdoch Childrens Res Inst Melbourne Australia Univ Melbourne Dept Paediat Melbourne Australia Sydney Childrens Hosp Kids Canc Ctr High St Randwick NSW 2031 Australia Univ Ghent Ctr Med Genet Ghent Ghent Belgium Chinese Acad Sci Shenzhen Inst Adv Technol Shenzhen Peoples R China Univ Sydney Fac Sci Sch Life & Environm Sci Sydney NSW Australia UNSW Sydney Sch Clin Med UNSW Med & Hlth Kensington NSW Australia Univ Newcastle Prior Res Ctr Canc Res Sch Med & Publ Hlth Callaghan NSW 2308 Australia

Tumorigenic drivers of MYCN gene nonamplified neuroblastoma remain largely uncharacterized. long noncoding rnas (lncrnas) regulate tumorigenesis, however, there is little literature on therapeutic targeting of lncrnas with small molecule compounds. Here PRKCQ-AS1 is identified as the lncrna most overexpressed in MYCN nonamplified, compared with MYCN-amplified, neuroblastoma cell lines. PRKCQ-AS1 expression is controlled by super-enhancers, and PRKCQ-AS1 rna bound to MSI2 protein. rna immunoprecipitation and sequencing identified BMX mrna as the transcript most significantly disrupted from binding to MSI2 protein, after PRKCQ-AS1 knockdown. PRKCQ-AS1 or MSI2 knockdown reduces, while its overexpression enhances, BMX mrna stability and expression, ERK protein phosphorylation and MYCN nonamplified neuroblastoma cell proliferation. PRKCQ-AS1 knockdown significantly suppresses neuroblastoma progression in mice. In human neuroblastoma tissues, high levels of PRKCQ-AS1 and MSI2 expression correlate with poor patient outcomes, independent of current prognostic markers. AlphaScreen of a compound library identifies NSC617570 as an efficient inhibitor of PRKCQ-AS1 rna and MSI2 protein interaction, and NSC617570 reduces BMX expression, ERK protein phosphorylation, neuroblastoma cell proliferation in vitro and tumor progression in mice. The study demonstrates that PRKCQ-AS1 rna interacts with MSI2 protein to induce neuroblastoma tumorigenesis, and that targeting PRKCQ-AS1 and MSI2 interaction with small molecule compounds is an effective anticancer strategy.

关键词： long noncoding rna long noncoding rna inhibitor Neuroblastoma rna binding protein small molecule compounds tumorigenesis

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Wenshen Yiqi Granule Alleviates Chronic Obstructive Pulmonary Disease via the long noncoding rna-XIST/Microrna-200c-3p Axis

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PULMONARY CIRCULATION 2025年第1期15卷 e70040页

作者： Deng, Haoran Zhu, Shiping Yu, Fei Song, Xue Jin, Xinlai Ding, Xuchun Zhejiang Chinese Med Univ Dept Resp & Crit Care Med Hangzhou TCM Hosp Hangzhou Peoples R China

Chronic obstructive pulmonary disease (COPD) is a major challenge to global public health. Evidence showed that long noncoding rna (lncrna)-XIST/microrna (mirna)-200c-3p axis regulated apoptosis and inflammation in cigarette smoke extract (CSE)-exposed human bronchial epithelial cells. Wenshen Yiqi granule (WSYQG) is a Traditional Chinese medicine compound prescription and often used for treating COPD. However, the current understanding of the mechanism by which WSYQG improves COPD is still limited, which has somewhat restrained its widespread application. Therefore, this study aims to investigate the effects and biological mechanisms of WSYQG on CSE-exposed type II alveolar epithelial (AEC II) cells with cell transfection and mirna mimics/inhibitors intervention. Cell counting kit-8, flow cytometry, Transwell, Western blot, real-time quantitative reverse transcription PCR, and fluorescence in situ hybridization assays were used. Results showed that WSYQG intervention increased cell viability and decreased levels of IFN-gamma, TNF-alpha and apoptosis, also preventing cell migration in CSE-exposed ACE II cells. Additionally, expression of epithelial marker (ZO-1), Notch1/4 decreased, and mesenchymal markers (vimentin) and Notch2 expression increased in CSE-exposed ACE II cells, while WSYQG intervention antagonized them and also decreased N-cadherin and increased E-cadherin. Silencing lncrna-XIST enhanced WSYQG's effects on CSE-exposed ACE II cells, while inhibiting miR-200c-3p reversed silencing lncrna-XIST's effects. Furthermore, dual-luciferase reporter assay system and rna immunoprecipitation assay proved that lncrna-XIST acts as a miR-200c-3p sponge. This study highlights the importance of the lncrna-XIST/miR-200c-3p axis in WSYQG improving COPD, providing a research basis for WSYQG to improve COPD and expanding the possibility of expanding its clinical application.

关键词： epithelial mesenchymal transition long noncoding rna microrna Notch primary culture

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Analysis of long noncoding rna in Fatty Acid Metabolism to Identify Prognostic Markers and Predict Immunotherapy Response in Low-Grade Glioma

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World Neurosurgery 2025年 196卷 123723-123723页

作者： Cui, Yang Department of Neurosurgery Hebei Yanda Hospital He Bei Langfang China

Background: Low-grade gliomas (LGGs) are notorious for their difficult early-stage diagnosis, limited treatment options, and poor prognosis, making them a focal point in cancer research. long noncoding rnas (lncrnas) have been identified as regulators of metabolic reprogramming in tumor cells, offering new directions for LGG treatment. Methods: This study employed data from The Cancer Genome Atlas, focusing on key fatty acid metabolism-related lncrna. A risk scoring model was developed using univariate/multifactorial and least absolute shrinkage and selection operator Cox regression. Additionally, the study evaluated the role of these prognostic lncrnas in LGG progression by assessing associations between LGG immune markers and tumor drug resistance. Finally, functional enrichment analysis highlighted the molecular roles of these lncrnas. Results: In this study, a total of 14 prognostic lncrnas were obtained. The risk model demonstrated excellent validity and reliability, making it a superior predictor of prognosis among patients with varying LGG risks. Among the identified lncrnas, GHET-1 was notably associated with LGG sensitivity to current chemotherapy options and might be a crucial lncrna affecting LGG progression. High-risk patients exhibited T-helper cell-mediated immunosuppression, potentially paving new paths for future LGG immunotherapy. Conclusions: Focusing on lncrna regulation and fatty acid metabolism reprogramming, this study established an innovative prognostic prediction model for LGGs, showing outstanding validity and reliability. The findings offer new molecular and cellular targets for the future development of LGG treatments. © 2025 The Author(s)

关键词： Fatty acid metabolism Immune cells long noncoding rna Low-grade gliomas

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