Human Cell最新文献_第5页

METTL3 promotes m6A hypermethylation of RBM14 via YTHDF1 leading to the progression of hepatocellular carcinoma. METTL3通过YTHDF1促进RBM14的m6A超甲基化，导致肝细胞癌的进展。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-10 DOI: 10.1007/s13577-022-00769-3

Jingyao Hu, Liang Yang, Xueqiang Peng, Minghuan Mao, Xiaodan Liu, Jianbo Song, Hangyu Li, Fu Chen

{"title":"METTL3 promotes m6A hypermethylation of RBM14 via YTHDF1 leading to the progression of hepatocellular carcinoma.","authors":"Jingyao Hu, Liang Yang, Xueqiang Peng, Minghuan Mao, Xiaodan Liu, Jianbo Song, Hangyu Li, Fu Chen","doi":"10.1007/s13577-022-00769-3","DOIUrl":"10.1007/s13577-022-00769-3","url":null,"abstract":"Liver is a well-known immunological organ with unique microenvironment. In normal conditions, the rich immune-infiltrating cells cooperate with non-parenchymal cells, such as Kupffer cells (KCs). The presence of liver immunosuppressive microenvironment underlines the importance to dissect this interaction to understand how this cross-talk promotes tumor growth in hepatocellular carcinoma (HCC). Therefore, the aim of the study here was to probe the role of methyltransferase-like 3 (METTL3) in the HCC progression and its effect on the polarization of KCs. KCs showed M2 polarization, and METTL3 was overexpressed in our collected HCC tissues relative to adjacent tissues. METTL3 depletion inhibited the M2 polarization of KCs, thereby reverting the malignant phenotype of HCC cells in vitro and growth and metastasis in vivo. Mechanistically, YTH domain-containing family protein 1 (YTHDF1) bound to RNA-binding protein 14 (RBM14), whereas METTL3 knockdown in KCs cells suppressed RBM14 expression by decreasing N-methyladenosine (m6A) methylation. Overexpression of RBM14 mitigated the anti-tumor effects of sh-METTL3 in vitro and in vivo. It is suggested that the mechanism of sh-METTL3 suppressing the polarization of KCs and the progression of HCC is to regulate the RBM14 expression via YTHDF1-dependent m6A modification.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":" ","pages":"1838-1855"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33458313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FOSL2 deficiency delays nonalcoholic steatohepatitis progression by regulating LY6D-mediated NLRP3 activation. FOSL2缺乏通过调节ly6d介导的NLRP3激活来延缓非酒精性脂肪性肝炎的进展。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-05 DOI: 10.1007/s13577-022-00760-y

Pei-Xin Hu, Mei-Yan Sheng, Yan-Ping Liu, Chun-Qing Zhang

{"title":"FOSL2 deficiency delays nonalcoholic steatohepatitis progression by regulating LY6D-mediated NLRP3 activation.","authors":"Pei-Xin Hu, Mei-Yan Sheng, Yan-Ping Liu, Chun-Qing Zhang","doi":"10.1007/s13577-022-00760-y","DOIUrl":"10.1007/s13577-022-00760-y","url":null,"abstract":"Lymphocyte antigen 6 family member D (LY6D) was enhanced specifically in senescent cells, while its effects on pyroptosis, a programmed cell death, remains unknown. The goal of this study was to assess the role of LY6D in the mediation of pyroptosis during nonalcoholic steatohepatitis (NASH). After screening out LY6D as a specific liver fibrosis-associated gene using the GSE55747 dataset from the GEO database, we established a NASH mouse model using methionine and choline deficient-diet feeding and an in vitro model using lipopolysaccharide (LPS)-treated hepatocytes. LY6D was overexpressed in NASH livers as well as in LPS-treated hepatocytes. Silencing of LY6D inhibited NASH-associated hepatocyte pyroptosis. With the aid of bioinformatics analysis, promoter-luciferase reporter and ChIP-qPCR assays, we identified FOSL2 as an upstream transcription factor of LY6D. FOSL2, which was highly expressed in NASH, promoted LY6D transcription by binding to the promoter of LY6D. Depletion of FOSL2 significantly inhibited NASH-associated hepatocyte pyroptosis, which was significantly reversed after overexpression of LY6D. Moreover, the promotion of hepatocyte pyroptosis by the FOSL2/LY6D axis was significantly attenuated by specific inhibition of NLRP3. These findings suggesting that FOSL2/LY6D axis may be a key molecular axis and a potential target for NASH therapeutics.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1752-1765"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40584186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNF126 contributes to stem cell-like properties and metastasis in hepatocellular carcinoma through ubiquitination and degradation of LKB1. RNF126通过泛素化和LKB1降解参与肝细胞癌的干细胞样特性和转移。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-06 DOI: 10.1007/s13577-022-00782-6

Jie Huang, Yan Li, Mengyao Zheng, Haiyu He, Dingwei Xu, Daguang Tian

{"title":"RNF126 contributes to stem cell-like properties and metastasis in hepatocellular carcinoma through ubiquitination and degradation of LKB1.","authors":"Jie Huang, Yan Li, Mengyao Zheng, Haiyu He, Dingwei Xu, Daguang Tian","doi":"10.1007/s13577-022-00782-6","DOIUrl":"10.1007/s13577-022-00782-6","url":null,"abstract":"Hepatocellular carcinoma (HCC) is one of the malignant tumors with the worst prognosis, and tumor recurrence and metastasis are the main factors leading to poor prognosis of HCC patients. Accumulating studies show that RNF126, ring finger protein 126, is involved in the pathological process of many tumors. However, the biological function and exact molecular mechanism of RNF126 in HCC remain unclear. In this study, we investigated the role of RNF126 in the pathogenesis of HCC. By analyzing database and verifying with our clinical specimens, it was found that RNF126 was highly expressed in HCC tissues, which is associated with shorter overall survival and higher recurrence rate. Overexpressed RNF126 can significantly promote the proliferation, migration, invasion and angiogenesis of HCC cells, whereas knockdown RNF126 can reverse this effect. Mechanically, RNF126 down-regulates liver kinase B1 (LKB1) expression by ubiquitination of LKB1 to weaken its stability, thereby significantly promoting stem-cell-like activity, migration, and angiogenesis of HCC. Notably, consistent with in vitro results, RNF126 was stably transformed in Hep3B and subcutaneously injected into nude mice. In established mouse xenograft models, tumor growth can be effectively inhibited and the occurrence of lung metastasis is reduced. In HCC, RNF126 may down-regulate LKB1 through ubiquitination, thus becoming a powerful prognostic biomarker and a recognized tumor suppressor. Therefore, our study may provide a promising new therapeutic strategy for targeting RNF126 for HCC patients.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1869-1884"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40353551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MicroRNA-149-3p expression correlates with outcomes of adrenocortical tumor patients and affects proliferation and cell cycle progression of H295A adrenocortical cancer cell line. MicroRNA-149-3p的表达与肾上腺皮质肿瘤患者的预后相关，影响H295A肾上腺皮质癌细胞系的增殖和细胞周期进展。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-02 DOI: 10.1007/s13577-022-00778-2

Keteryne Rodrigues da Silva, Luciana Chain Veronez, Carolina Alves Pereira Correa, Régia Caroline Peixoto Lira, Mirella Baroni, Rosane de Paula Silva Queiroz, Sonir Roberto Rauber Antonini, José Andres Yunes, Silvia Regina Brandalise, Luiz Gonzaga Tone, Carlos Alberto Scrideli

{"title":"MicroRNA-149-3p expression correlates with outcomes of adrenocortical tumor patients and affects proliferation and cell cycle progression of H295A adrenocortical cancer cell line.","authors":"Keteryne Rodrigues da Silva, Luciana Chain Veronez, Carolina Alves Pereira Correa, Régia Caroline Peixoto Lira, Mirella Baroni, Rosane de Paula Silva Queiroz, Sonir Roberto Rauber Antonini, José Andres Yunes, Silvia Regina Brandalise, Luiz Gonzaga Tone, Carlos Alberto Scrideli","doi":"10.1007/s13577-022-00778-2","DOIUrl":"10.1007/s13577-022-00778-2","url":null,"abstract":"Pediatric adrenocortical tumor (ACT) is a rare and aggressive neoplasm, with incidence in southern and southeastern Brazil 10-15 times higher than worldwide. Although microRNAs (miRNAs) have been reported to act as tumor suppressors or oncogenes in several cancers, the role of miR-149-3p in ACT remains unknown. In this study, we evaluated the expression of miR-149-3p in 67 pediatric ACT samples and 19 non-neoplastic adrenal tissues. The overexpression of miR-149-3p was induced in H295A cell line, and cell viability, proliferation, colony formation, and cell cycle were assessed by in miR-149-3p mimic or mimic control. In silico analysis were used to predict miR-149-3p putative target genes. CDKN1A expression at the mRNA and protein levels was evaluated by qRT-PCR and western blot, respectively. Higher miR-149-3p expression was associated with unfavorable ACT outcomes. Compared to the mimic control, miR-149-3p overexpression increased cell viability and colony formation, and affected cell cycle progression. Also, we identified CDKN1A as a potential miR-149-3p target gene, with decreased expression at both the gene and protein levels in miR-149-3p mimic cells. Collectively, these findings suggest that miR-149-3p promotes H295A cell viability by downregulating CDKN1A and provide evidence that miR-149-3p may be useful as a novel therapeutic target for pediatric ACT.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1952-1960"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: Downregulation of miR-96 suppresses the profibrogenic functions of cardiac fibroblasts induced by angiotensin II and attenuates atrial fibrosis by upregulating KLF13. 注:miR-96下调可抑制血管紧张素II诱导的心脏成纤维细胞的促纤维化功能，并通过上调KLF13减轻心房纤维化。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 DOI: 10.1007/s13577-022-00780-8

Lijie Su, Yili Yao, Wei Song

引用次数: 1

Pyroptosis: a novel signature to predict prognosis and immunotherapy response in gliomas. 焦下垂：预测胶质瘤预后和免疫治疗反应的新特征。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-21 DOI: 10.1007/s13577-022-00791-5

Guiying He, Zhimin Chen, Shenghua Zhuo, Jingzhi Tang, Weijie Hao, Kun Yang, Chunshui Yang

{"title":"Pyroptosis: a novel signature to predict prognosis and immunotherapy response in gliomas.","authors":"Guiying He, Zhimin Chen, Shenghua Zhuo, Jingzhi Tang, Weijie Hao, Kun Yang, Chunshui Yang","doi":"10.1007/s13577-022-00791-5","DOIUrl":"10.1007/s13577-022-00791-5","url":null,"abstract":"Gliomas are the most common primary brain tumors and are highly malignant with a poor prognosis. Pyroptosis, an inflammatory form of programmed cell death, promotes the inflammatory cell death of cancer. Studies have demonstrated that pyroptosis can promote the inflammatory cell death (ICD) of cancer, thus affecting the prognosis of cancer patients. Therefore, genes that control pyroptosis could be a promising candidate bio-indicator in tumor therapy. The function of pyroptosis-related genes (PRGs) in gliomas was investigated based on the Chinese Glioma Genome Atlas (CGGA), the Cancer Genome Atlas (TCGA) and the Repository of Molecular Brain Neoplasia Data (Rembrandt) databases. In this study, using the non-negative matrix factorization (NMF) clustering method, 26 PRGs from the RNA sequencing data were divided into two subgroups. The LASSO and Cox regression was used to develop a 4-gene (BAX, Caspase-4, Caspase-8, PLCG1) risk signature, and all glioma patients in the CGGA, TCGA and Rembrandt cohorts were divided into low- and high-risk groups. The results demonstrate that the gene risk signature related to clinical features can be used as an independent prognostic indicator in glioma patients. Moreover, the high-risk subtype had rich immune infiltration and high expression of immune checkpoint genes in the tumor immune microenvironment (TIME). The analysis of the Submap algorithm shows that patients in the high-risk group could benefit more from anti-PD1 treatment. The risk characteristics associated with pyroptosis proposed in this study play an essential role in TIME and can potentially predict the prognosis and immunotherapeutic response of glioma patients.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1976-1992"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40371669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: Long non-coding RNA VPS9D1-AS1 promotes growth of colon adenocarcinoma by sponging miR-1301-3p and CLDN1. 注:长链非编码RNA VPS9D1-AS1通过海绵作用miR-1301-3p和CLDN1促进结肠腺癌生长。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 DOI: 10.1007/s13577-022-00784-4

Wei Liu

引用次数: 2

Establishment and characterization of NCC-MRT1-C1: a novel cell line of malignant rhabdoid tumor. 恶性横纹肌样瘤新细胞系NCC-MRT1-C1的建立与表征。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-05 DOI: 10.1007/s13577-022-00751-z

Taro Akiyama, Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Chiaki Sato, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Seji Ohtori, Tadashi Kondo

{"title":"Establishment and characterization of NCC-MRT1-C1: a novel cell line of malignant rhabdoid tumor.","authors":"Taro Akiyama, Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Chiaki Sato, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Seji Ohtori, Tadashi Kondo","doi":"10.1007/s13577-022-00751-z","DOIUrl":"https://doi.org/10.1007/s13577-022-00751-z","url":null,"abstract":"Malignant rhabdoid tumor (MRT) is a sarcoma histologically characterized by rhabdoid cells and genetically characterized by loss of function of the chromatin remodeling complex SWI/SNF induced by SMARCB1 gene deficiency. MRT mainly occurs in children, may arise in various locations, but is predominantly in the central nervous system (CNS) and kidney. Although MRT exhibits poor prognosis, standard treatment has not yet been established due to its extreme rarity. Patient-derived cancer cell lines are critical tools for basic and pre-clinical research in the development of chemotherapy. However, none of the MRT cell lines was derived from adult patients, and only one cell line was derived from the MRT of a soft tissue, despite the clinical behavior of MRT varying according to patient age and anatomic site. Herein, we reported the first cell line of MRT isolated from the soft tissue of an adult patient and named it NCC-MRT1-C1. NCC-MRT1-C1 cells showed a biallelic loss of the SMARCB1 gene. NCC-MRT1-C1 cells demonstrated rapid proliferation, spheroid formation, invasion capability in vitro, and tumorigenesis in nude mice. Screening of antitumor agents in NCC-MRT1-C1 cells resulted in the identification of six effective drugs. In conclusion, we report the first MRT cell line from the soft tissue of an adult patient. We believe that NCC-MRT1-C1 is a useful tool for developing novel chemotherapies for MRT.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"2002-2010"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40694325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of PYCR1 in inhibiting 5-fluorouracil-induced ferroptosis and apoptosis through SLC25A10 in colorectal cancer. PYCR1在结直肠癌中通过SLC25A10抑制5-氟尿嘧啶诱导的铁氧化和细胞凋亡的作用

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-14 DOI: 10.1007/s13577-022-00775-5

Borong Zhou, Zhongchao Mai, Ying Ye, Yanan Song, Miao Zhang, Xinlin Yang, Wei Xia, Xiaofeng Qiu

{"title":"The role of PYCR1 in inhibiting 5-fluorouracil-induced ferroptosis and apoptosis through SLC25A10 in colorectal cancer.","authors":"Borong Zhou, Zhongchao Mai, Ying Ye, Yanan Song, Miao Zhang, Xinlin Yang, Wei Xia, Xiaofeng Qiu","doi":"10.1007/s13577-022-00775-5","DOIUrl":"10.1007/s13577-022-00775-5","url":null,"abstract":"Although PYCR1 is a well-recognized oncogenic gene for malignant tumors, the causal relationship of its expression with malignant growth and cytotoxic chemotherapeutics remains unclear. Therefore, this study aimed to clarify the role of PYCR1 and its interaction with SLC25A10 in a chemotherapeutic agent 5-fluorouracil (5-FU)'s toxicity to colorectal cancer cells. PYCR1 and SLC25A10 expressions were detected in The Cancer Genome Atlas database and colon adenocarcinoma (COAD) clinical samples. PYCR1 upregulation was associated with SLC25A10 expression and poor prognosis, and its high expression indicated decreased survival rates in patients with COAD. PYCR1 overexpression inhibited lipid reactive oxygen species production and promoted SLC25A10 expression in colorectal cancer cells. PYCR1 silencing enhanced the antitumor effects of 5-FU. Ferroptosis inhibitor deferoxamine suppressed the antitumor effects of PYCR1 silencing, whereas ferroptosis inducer erastin inhibited the protumor effects of PYCR1 overexpression. SLC25A10 overexpression reversed the antitumor effects of PYCR1 silencing in vitro and inhibited the antitumor effects of erastin in vivo. Therefore, PYCR1 is an oncogenic gene that promotes colorectal tumor growth and desensitizes colorectal cancer cells to 5-FU cytotoxicity by preventing apoptosis and ferroptosis.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1900-1911"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40357103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Long non-coding RNA RPL34-AS1 ameliorates oxygen-glucose deprivation-induced neuronal injury via modulating miR-223-3p/IGF1R axis. 长链非编码RNA RPL34-AS1通过调节miR-223-3p/IGF1R轴改善氧葡萄糖剥夺诱导的神经元损伤。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-25 DOI: 10.1007/s13577-022-00773-7

Xin-Ya Wei, Tian-Qi Zhang, Rui Suo, You-Yang Qu, Yan Chen, Yu-Lan Zhu

{"title":"Long non-coding RNA RPL34-AS1 ameliorates oxygen-glucose deprivation-induced neuronal injury via modulating miR-223-3p/IGF1R axis.","authors":"Xin-Ya Wei, Tian-Qi Zhang, Rui Suo, You-Yang Qu, Yan Chen, Yu-Lan Zhu","doi":"10.1007/s13577-022-00773-7","DOIUrl":"10.1007/s13577-022-00773-7","url":null,"abstract":"Ribosomal protein L34-antisense RNA 1 (RPL34-AS1), one of the long non-coding RNAs (lncRNAs), plays an important function in regulating diverse human malignant tumors. Nevertheless, the functions of RPL34-AS1 in ischemic stroke remain unclear. The present work focused on determining the candidate targets of RPL34-AS1 and its related mechanism in ischemic injury. The oxygen-glucose deprivation (OGD/R) in vitro cell model and middle cerebral artery occlusion (MCAO) in vivo rat model were utilized to simulate the pathological process of ischemic stroke. Additionally, the CCK8, WB (detecting Bcl-2 and Bax protein levels), and caspase-3 activity assays were done to investigate the anti-apoptotic functions of RPL34-AS1. The relationship among RPL34-AS1, insulin-like growth factor 1 receptor (IGF1R), and microRNA-223-3p (miR-223-3p) was determined through luciferase reporter assay. In this study, RPL34-AS1 expression was reduced in patients suffering from ischemic stroke. The overexpression of RPL34-AS1 reduced ischemic brain damage. However, the cell viability and glucose uptake were increased, and the apoptosis rate was decreased in the OGD/R-induced neurons. Further, miR-223-3p resulted in the decreased cell viability and glucose uptake and the increased cell apoptosis to cause ischemic brain damage. Besides, the neuroprotective effects of RPL34-AS1 on OGD/R injury were partly reversed by miR-223-3p. Mechanistically, lncRNA RPL34-AS1 could function as the competing endogenous RNA (ceRNA) of miR-223-3p to regulate IGF1R. Collectively, our study demonstrated that lncRNA RPL34-AS1 attenuated OGD/R-induced neuronal injury by mediating miR-223-3p/IGF1R axis. This discovery might serve as the candidate therapeutic target for ischemic stroke.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1785-1796"},"PeriodicalIF":2.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40427075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0