scholarly journals Peptidome Analysis of Cerebrospinal Fluid in Neonates with Hypoxic-Ischemic Brain Damage

2020 ◽  
Author(s):  
Xuewen Hou ◽  
Zijun Yuan ◽  
Xuan Wang ◽  
Rui Cheng ◽  
Xiaoguang Zhou ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Expression Profiles ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Glucose Deprivation ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Control Group ◽  
Ischemic Brain ◽  
Caspase 1

Abstract Hypoxic-ischemic brain injury (HIBD) causes neonatal death and serious neurological disability; however, there are currently no promising therapies for it excepting cooling. Therefore, in this study, we used peptidome analysis to identify differentially expressed peptides in cerebrospinal fluid (CSF) of neonates with HIBD or controls, which may give a foundation for finding new promising drugs of neonatal HIBD. CSF samples were collected from neonates with HIBD (n = 4) or controls (n = 4). ITRAQ LC-MS/MS was used to identify differentially expressed peptides between two groups. Effects of the peptide from heat shock protein 90-alpha (HSP90α/HSP90AA1) on cell viability and pyroptosis under oxygen and glucose deprivation (OGD) were analyzed using cell counting kit-8 (CCK-8) assay and Annexin V-fluorescein isothiocyanate (FITC) Assay. Expressions of NLRP3, ASC and Caspase-1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Compared with the control group, one peptide significantly up-regulated and thirty-four peptides significantly down-regulated in the CSF of neonates with HIBD. A fragment of HSP90α/HSP90AA1 is the 2671.5 Da peptide (HSQFIGYPITLFVEKER), one of the down-regulated peptides in neonatal HIBD. This peptide, we named it HIBDAP, inhibited pyroptosis of PC12 cells under OGD by suppressing expressions of NLRP3, ASC and Caspase-1. The results of our study identified the characterization and expression profiles of peptides in CSF of neonatal HIBD. Several meaningful peptides such as HIBDAP may play significant roles in neonatal HIBD and may provide new therapeutic targets for neonatal HIBD.

scholarly journals Peptidome analysis of cerebrospinal fluid in neonates with hypoxic-ischemic brain damage

2020 ◽  
Author(s):  
Xuewen Hou ◽  
Zijun Yuan ◽  
Xuan Wang ◽  
Rui Cheng ◽  
Xiaoguang Zhou ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Expression Profiles ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Glucose Deprivation ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Control Group ◽  
Ischemic Brain ◽  
Caspase 1

Abstract Hypoxic-ischemic brain injury (HIBD) causes neonatal death and serious neurological disability; however, there are currently no promising therapies for it excepting cooling. Therefore, in this study, we used peptidome analysis to identify differentially expressed peptides in cerebrospinal fluid (CSF) of neonates with HIBD or controls, which may give a foundation for finding new promising drugs of neonatal HIBD. CSF samples were collected from neonates with HIBD (n=4) or controls (n=4). ITRAQ LC-MS/MS was used to identify differentially expressed peptides between two groups. Effects of the peptide from heat shock protein 90-alpha (HSP90α/HSP90AA1) on cell viability and pyroptosis under oxygen and glucose deprivation (OGD) were analyzed using cell counting kit-8 (CCK-8) assay and Annexin V-fluorescein isothiocyanate (FITC) Assay. Expressions of NLRP3, NLRP1, ASC and Caspase-1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Compared with the control group, one peptide significantly up-regulated and thirty-four peptides significantly down-regulated in the CSF of neonates with HIBD. A fragment of HSP90α/HSP90AA1 is the 2671.5Da peptide (HSQFIGYPITLFVEKER), one of the down-regulated peptides in neonatal HIBD. This peptide, we named it HIBDAP, inhibited pyroptosis of PC12 cells under OGD by suppressing expressions of NLRP3, ASC and Caspase-1 except NLRP1. The results of our study identified the characterization and expression profiles of peptides in CSF of neonatal HIBD. Several meaningful peptides such as HIBDAP may play significant roles in neonatal HIBD and provide new therapeutic targets for neonatal HIBD.

scholarly journals Peptidome analysis of cerebrospinal fluid in neonates with hypoxic-ischemic brain damage

2020 ◽  
Author(s):  
Xuewen Hou ◽  
Zijun Yuan ◽  
Xuan Wang ◽  
Rui Cheng ◽  
Xiaoguang Zhou ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pc12 Cells ◽  
Brain Damage ◽  
Expression Profiles ◽  
Heat Shock Protein 90 ◽  
Differentially Expressed ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Protein Protein Interaction ◽  
Hydrophilic Peptide

Abstract Hypoxic-ischemic brain injury (HIBD) causes neonatal death and serious neurological disability; however, there are currently no promising therapies for it excepting cooling. Therefore, in this study, we used peptidome analysis to identify differentially expressed peptides in cerebrospinal fluid (CSF) of neonates with HIBD or controls, which may give a foundation for finding new promising drugs of neonatal HIBD. CSF samples were collected from neonates with HIBD (n=4) or controls (n=4). ITRAQ LC-MS/MS was used to identify differentially expressed peptides between two groups. A total of 35 differentially expressed peptides from 25 precursor proteins were identified. The 2671.5Da peptide (HSQFIGYPITLFVEKER), one of the down-regulated peptides in neonatal HIBD, is a fragment of heat shock protein 90-alpha (HSP90α/HSP90AA1). Results of bioinformatics analysis showed that HSP90α/HSP90AA1 was located in the protein-protein interaction (PPI) network hub and was involved in the NOD-LIKE receptor (NLR) signaling pathway. This peptide, we named it HIBDAP (Hypoxic-Ischemic Brain Damage Associated Peptide), is a hydrophilic peptide with high stability and has a long half-life of 3.5h in mammalian reticulocytes. It was demonstrated that TAT-HIBDAP could successfully enter PC12 cells and further into the nucleus. After HIBDAP pretreatment and 6 hours of OGD treatment, low concentrations of HIBDAP increased the survival rate of cells, except 40μM had a toxic effect. Safe concentrations of HIBDAP reduced pyroptosis of PC12 cells under OGD, except 20μM had no effect, by suppressing expressions of NLRP3, ASC and Caspase-1 except NLRP1. The results of our study identified the characterization and expression profiles of peptides in CSF of neonatal HIBD. Several meaningful peptides such as HIBDAP may play significant roles in neonatal HIBD and provide new therapeutic targets for neonatal HIBD.

scholarly journals Peptidome analysis of cerebrospinal fluid in neonates with hypoxic-ischemic brain damage

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Xuewen Hou ◽  
Zijun Yuan ◽  
Xuan Wang ◽  
Rui Cheng ◽  
Xiaoguang Zhou ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pc12 Cells ◽  
Brain Damage ◽  
Expression Profiles ◽  
Heat Shock Protein 90 ◽  
Differentially Expressed ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Protein Protein Interaction ◽  
Hydrophilic Peptide

Abstract Hypoxic-ischemic brain injury (HIBD) causes neonatal death and serious neurological disability; however, there are currently no promising therapies for it excepting cooling. Therefore, in this study, we used peptidome analysis to identify differentially expressed peptides in cerebrospinal fluid (CSF) of neonates with HIBD or controls, which may give a foundation for finding new promising drugs of neonatal HIBD. CSF samples were collected from neonates with HIBD (n = 4) or controls (n = 4). ITRAQ LC–MS/MS was used to identify differentially expressed peptides between two groups. A total of 35 differentially expressed peptides from 25 precursor proteins were identified. The 2671.5 Da peptide (HSQFIGYPITLFVEKER), one of the down-regulated peptides in neonatal HIBD, is a fragment of heat shock protein 90-alpha (HSP90α/HSP90AA1). Results of bioinformatics analysis showed that HSP90α/HSP90AA1 was located in the protein–protein interaction (PPI) network hub and was involved in the NOD-LIKE receptor (NLR) signaling pathway. This peptide, we named it Hypoxic-Ischemic Brain Damage Associated Peptide (HIBDAP), is a hydrophilic peptide with high stability and has a long half-life of 3.5 h in mammalian reticulocytes. It was demonstrated that TAT-HIBDAP could successfully enter PC12 cells and further into the nucleus. After HIBDAP pretreatment and 6 h of OGD treatment, low concentrations of HIBDAP increased the survival rate of cells, except 40 μM had a toxic effect. Safe concentrations of HIBDAP reduced pyroptosis of PC12 cells under OGD, except 20 μM had no effect, by suppressing expressions of NLRP3, ASC and Caspase-1 except NLRP1. The results of our study identified the characterization and expression profiles of peptides in CSF of neonatal HIBD. Several meaningful peptides such as HIBDAP may play significant roles in neonatal HIBD and provide new therapeutic targets for neonatal HIBD.

Indole-3-carbinol inhibits the proliferation of colorectal carcinoma LoVo cells through activation of the apoptotic signaling pathway

2021 ◽  
pp. 096032712110214
Author(s):  
JY Lee ◽  
HM Lim ◽  
CM Lee ◽  
S-H Park ◽  
MJ Nam
Keyword(s):  
Colorectal Carcinoma ◽  
Cancer Cells ◽  
Inhibitory Activity ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Cell Counting ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Lovo Cells

Indole-3-carbinol (I3C) is a phytochemical that exhibits growth-inhibitory activity against various cancer cells. However, there are limited studies on the effects of I3C on colon cancer cells. In this study, the growth-inhibitory activity of I3C against the human colorectal carcinoma cell line (LoVo) was examined. The results of the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide, colony formation, and cell counting assays revealed that I3C suppressed the proliferation of LoVo cells. Microscopy and wound-healing analyses revealed that I3C affected the morphology and inhibited the migration of LoVo cells, respectively. I3C induced apoptosis and DNA fragmentation as evidenced by the results of fluorescein isothiocyanate-conjugated annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay, respectively. Additionally, I3C arrested the cell cycle at the G0/G1 phase and enhanced the reactive oxygen species levels. Western blotting analysis revealed that treatment with I3C resulted in the activation of apoptotic proteins, such as poly(ADP-ribose) polymerase, caspase-3, caspase-7, caspase-9, Bax, Bim, and p53 in LoVo cells. These results indicate that I3C induces apoptosis in LoVo cells by upregulating p53, leading to the activation of Bax and caspases. Taken together, I3C exerts cytotoxic effects on LoVo cells by activating apoptosis.

Abstract TMP23: Inflammasome-derived Caspase-1 is Elevated in the Cerebrospinal Fluid of Subarachnoid Hemorrhage Patients and Correlated to Outcome

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yonatan Hirsch ◽  
Joseph R Geraghty ◽  
Eitan A Katz ◽  
Jeffrey A Loeb ◽  
Fernando Testai
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
External Ventricular Drain ◽  
Analysis Of Covariance ◽  
Control Group ◽  
Normal Brain ◽  
Poor Outcome ◽  
Caspase 1 ◽  
Initial Severity ◽  
Poor Outcomes

Introduction: The role of neuroinflammation following aneurysmal subarachnoid hemorrhage (SAH) and its relationship to outcome is the subject of many ongoing studies. The proteolytic enzyme, caspase-1, activated by the inflammasome complex, is known to contribute to numerous downstream pro-inflammatory effects. In this study, we investigated caspase-1 activity in the cerebrospinal fluid (CSF) of SAH patients and its association to outcome. Methods: SAH patients were recruited from a regional stroke referral center. CSF samples from 18 SAH subjects were collected via an external ventricular drain and obtained within 72 hours of the onset of symptoms. For control subjects, we collected the CSF from 9 patients undergoing lumbar puncture with normal CSF and normal brain MRI. Caspase-1 activity was measured using commercially available luminescence assays. SAH subjects were categorized at hospital discharge into those with good outcomes (Glasgow Outcome Scale, GOS, of 4-5) and poor outcomes (GOS of 1-3). The levels of caspase-1 activity in various groups were analyzed using Mann-Whitney and Pearson correlation tests. Caspase-1 activity was also adjusted by initial severity of bleed using analysis of covariance (ANCOVA). Results: Caspase-1 levels from SAH patients were significantly higher than that measured from the control group (mean 1.06x10-2 vs 1.90x10-3 counts per second (CPS)/μl*min), p = 0.0002). Within the SAH group, 10 patients (55.6%) had good outcomes and 8 patients (44.4%) had poor outcomes. Caspase-1 activity was significantly higher in the poor outcome group (mean 1.54x10-2 vs 1.60x10-3 CPS/μl*min), p = 0.0012). Additionally, caspase-1 activity had a statistically significant correlation with GOS score (r = -0.60; p = 0.0100). When adjusted for initial severity of bleed, the difference in caspase-1 activity in good vs. poor outcome remained significant (adjusted mean 7.10x10-3 vs. 2.54x10-2 CPS/μl*min, p=0.004). Conclusions: The inflammasome-dependent protein caspase-1 is elevated in CSF early after SAH and higher in those with poor functional outcome. Inflammasome activity therefore may serve as a novel biomarker to predict outcome shortly after aneurysm rupture.

scholarly journals The correlation between the granulocyte colony-stimulating factor and the Notch signaling pathway in ischemic brain injury

2021 ◽  
Author(s):  
Ning Xie ◽  
Qin Huang ◽  
Jingting Han ◽  
Wenyuan Xu
Keyword(s):  
Notch Pathway ◽  
Glucose Deprivation ◽  
Notch Signaling Pathway ◽  
Oxygen Glucose Deprivation ◽  
Control Group ◽  
Ischemic Brain Injury ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Ischemic Brain ◽  
Stimulating Factor

IntroductionThis study aims to determine the relationship between the granulocyte colony-stimulating factor (G-CSF) and the Notch signaling pathway in ischemic brain injury.Material and methodsPC-12 cells were treated with the nerve growth factor (NGF) to induce neuronal differentiation then divided into seven groups: 1) no treatment (control); 2) oxygen-glucose deprivation (OGD) model; 3) overexpressed G-CSF + OGD model; 4) transfected empty vector (negative control; NC) + OGD model; 5) overexpressed G-CSF + γ-secretase inhibitor MW167 + OGD model; 6) MW167 + OGD model; and 7) NC + MW167 + OGD model. The cells were analyzed using immunohistochemistry and apoptosis and CCK8 assays. The expression of the related molecules in the Notch pathway was detected using the Western blotting and quantitative PCR (Q-PCR).ResultsMost PC-12 cells were neuron-specific enolase (NSE)-positive after the NGF treatment. When compared with the control group, the MW167 + OGD and NC + MW167 + OGD groups had the lowest optical density (OD) values, followed by the OGD, NC + OGD and the G-CSF + MW167+ OGD groups. The G-CSF + OGD group had the highest OD value. Concerning apoptosis detection, the control group had the lowest apoptosis rate. The highest apoptosis rates were found in the MW167 + OGD, the OGD, and then the G-CSF + OGD groups.ConclusionsThe blocking of the Notch pathway can attenuate the G-CSF effects, whereas the G-CSF overexpression can activate the Notch pathway to resist the effects of oxygen-glucose deprivation.

scholarly journals Z-ligustilide protects BV-2 microglial cells against oxygen-glucose deprivation/reoxygenation-induced injury by inhibiting NLRP3 inflammasome activation and pyroptosis

2020 ◽  
Vol 18 ◽  
pp. 205873922093492
Author(s):  
Jia Hu ◽  
Jie Wei ◽  
Cheng Zeng ◽  
Fengqi Duan ◽  
Sijun Liu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Nlrp3 Inflammasome ◽  
Glucose Deprivation ◽  
Microglial Cells ◽  
Cell Counting ◽  
Oxygen Glucose Deprivation ◽  
Inflammasome Activation ◽  
Caspase 1 ◽  
Nlrp3 Inflammasome Activation ◽  
Active Caspase

Z-ligustilide (LIG) is the main bioactive compound of Danggui essential oil, which was reported to exert neuroprotective and anti-inflammatory effects. However, the underlying mechanism remains largely elusive. The present study aims to investigate the effect of LIG on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury and whether Nod-like receptor protein 3 (NLRP3) inflammasome and related pyroptosis are targets for the treatment of LIG. The OGD/R model was established in BV-2 microglial cells to investigate the protective effect of LIG. Cell viability and the release of lactate dehydrogenase (LDH) were determined by cell counting assay kit 8 and the LDH release assay kit. Western blot and immunofluorescence staining were carried out to detect NLRP3 inflammasome activation and pyroptosis. Active caspase-1 and TdT-mediated dUTP nick end labeling (TUNEL) double positive cells were defined as pyroptosis population. Statistical comparison among multiple groups was carried out by one-way analysis of variance (ANOVA) followed by least significant difference (LSD) test. Compared with control cells, OGD/R impaired cell viability and induced the release of LDH in BV-2 microglial cells, which were associated with the activation of NLRP3 inflammasome as evidenced by increased expression of NLRP3 and the cleavage of caspase-1 and interleukin-1 beta (IL-1β). In parallel with NLRP3 inflammasome activation, OGD/R induced pyroptotic cell death, manifested by the cleavage of gasdermin D (GSDMD) and increased population of active caspase-1+/TUNEL+ cells. All these events were significantly attenuated by treatment with LIG, indicating that LIG significantly inhibited NLRP3 inflammasome activation and pyroptosis, and ameliorated OGD/R-induced cell injury. In conclusion, LIG protects BV-2 microglial cells against OGD/R-induced injury via inhibition of NLRP3 inflammasome and pyroptosis.

NEDD4-1 Modulates the Resistance of Multiple Myeloma to Bortezomib

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2068-2068
Author(s):  
Xi Huang ◽  
Enfan Zhang ◽  
Xing Guo ◽  
Jing Chen ◽  
Xuanru Lin ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Lines ◽  
Conflicts Of Interest ◽  
Expression Profiles ◽  
Acquired Resistance ◽  
Gene Array ◽  
Cell Counting ◽  
Control Group ◽  
Protein Levels ◽  
Significant Difference

Abstract Background: Multiple myeloma (MM) is among the most common hematologic malignancies. Proteasome inhibitor bortezomib (Bor) is one of the most effective drugs for treatment of MM. However, during long-term Bor treatment, MM cells may eventually develop acquired-resistance to Bor which results in recurrence and a poor prognosis of MM. Several researches show that E3 ubiquitin ligases (E3s) primarily determine the substrate specificity of ubiquitin proteasome system and play an essential role in Bor resistance of MM. NEDD4-1 E3s, a founding member of the Neural precursor cell-Expressed Developmentally Downregulated gene 4 (NEDD4) family, was proved to involve in the proliferation, migration, invasion of cancer cells and the sensitivity of anticancer therapies. Our current study aims to explore the role and underlying mechanism of NEDD4-1 in acquired resistance of Bor in MM. Methods: The mRNA and protein levels of NEDD4-1 and its substrates in MM cell lines (H929, LP-1, RPMI8226, OPM-2 and ARP-1) and MM patients were detected by Quantitative Realtime PCR and Western Blotting. Lentiviral plasmids containing shRNA against NEDD4-1 were transfected into MM cells. Cell viability, proliferation and apoptosis of MM cells were measured by Cell Counting kit8 (CCK8) and flow cytometry. Gene array was used to compare the gene expression profiles of a panel of Bor treated MM cells vs vehicle-treated MM cells. Results: Gene array showed NEDD4-1 was significantly increased in MM cells treated with Bor. MM cells (CD138+ plasma cells of the bone marrow) from refractory/recurrence patients expressed lower NEDD4-1 than primary patient myeloma cells. Also, MM cell lines H929, ARP-1, LP-1 highly expressed NEDD4-1 at mRNA and protein levels. RPMI8226 and OPM-2 were relatively low expressed. Cell growth assay displayed no significant difference in proliferation between the NEDD4-1 knockdown (KD) and the control group (P>0.05). After suppression of NEDD4-1 using shRNAs, the killing effect of Bor in MM was significantly weaker than the control group (P<0.05). We also found that PTEN was decreased in the NEDD4-1 KD H929 cell line. Otherwise, phospho-STAT3 (ser727) and oncoprotein c-Myc and Bcl-2 were upregulated. Conclusion: Collectively, our study reveals that inhibition of NEDD4-1 can reduce MM sensitivity to Bor via regulating PTEN, c-Myc and Bcl-2, may be related to JAK/STAT signaling pathway, which suggests that NEDD4-1 probably acts as a novel drug target and therapeutic paradigm in the battle against multiple myeloma. Disclosures No relevant conflicts of interest to declare.

scholarly journals Comprehensive Analysis of the Profiles of Differentially Expressed mRNAs, lncRNAs, and circRNAs in Phosgene-Induced Acute Lung Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Yiru Shao ◽  
Zhifeng Jiang ◽  
Daikun He ◽  
Jie Shen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Therapeutic Potential ◽  
Expression Profiles ◽  
Mirna Gene ◽  
Differentially Expressed ◽  
Control Group ◽  
Group A ◽  
Group B ◽  
Air Control

Phosgene exposure can cause acute lung injury (ALI), for which there is no currently available effective treatment. Mesenchymal stem cells (MSCs) which have been proven to have therapeutic potential and be helpful in the treatment of various diseases, but the mechanisms underlying the function of MSCs against phosgene-induced ALI are still poorly explored. In this study, we compared the expression profiles of mRNAs, lncRNAs, and circRNAs in the lung tissues from rats of three groups—air control (group A), phosgene-exposed (group B), and phosgene + MSCs (group C). The results showed that 389 mRNAs, 198 lncRNAs, and 56 circRNAs were differently expressed between groups A and B; 130 mRNAs, 107 lncRNAs, and 35 circRNAs between groups A and C; and 41 mRNAs, 88 lncRNAs, and 18 circRNAs between groups B and C. GO and KEGG analyses indicated that the differentially expressed RNAs were mainly involved in signal transduction, immune system processes, and cancers. In addition, we used a database to predict target microRNAs (miRNAs) interacting with circRNAs and the R network software package to construct a circRNA-targeted miRNA gene network map. Our study showed new insights into changes in the RNA expression in ALI, contributing to explore the mechanisms underlying the therapeutic potential of MSCs in phosgene-induced ALI.

scholarly journals Differentially Expressed Long Noncoding RNAs Involved in FUBP1 Promoting Hepatocellular Carcinoma Cells Proliferation

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Xianpeng Li ◽  
Huaixi Yu ◽  
Feng Xu ◽  
Yifeng Wu ◽  
Jifang Sheng
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Noncoding Rna ◽  
Target Genes ◽  
Expression Profiles ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Rt Pcr ◽  
Upstream Element ◽  
Hcc Cells

Background. Far upstream element-binding protein 1 (FUBP1) is reported to be involved in cancer development by regulating the transcription of c-myc gene through binding to far upstream element. Highly expressed FUBP1 was negatively correlated with survival rate of patients with hepatocellular carcinoma (HCC) and could promote the proliferation of HCC cells. However, the downstream mechanism of FUBP1 has not yet been clearly explained. This study is aimed at identifying the expression profiles of long noncoding RNA (lncRNA) in HCC cells in response to FUBP1 overexpression and at investigating the possible lncRNAs that participated in cell proliferation process regulated by FUBP1. Methods. The overexpression of FUBP1 was mediated by lentiviral infection on 3 different types of HCC cell lines (MHCC97-H, MHCC97-L, and Huh-7). The expression of target genes was detected by quantitative reverse transcription-PCR (RT-PCR) and western blotting assays. Microarray and quantitative RT-PCR were applied to screen the differentially expressed lncRNAs in HCC cells after FUBP1 overexpression. The Cell Counting Kit-8 assay was used to confirm the growth vitality of HCC cells. Results. The growth vitality of HCC cells was significantly increased after lentivirus infection. A total of 12 lncRNAs had the same expression trend in the 3 HCC cell lines in response to FUBP1 overexpression, including 3 upregulated lncRNAs and 9 downregulated lncRNAs. Coexpression analysis of dysregulated lncRNAs-mRNAs network showed that lnc-LYZ-2 was the lncRNA most relevant to FUBP1. Inhibition of lnc-LYZ-2 could significantly relieve the proproliferation effect of FUBP1 on HCC cells, suggesting that lnc-LYZ-2 was partially involved in proproliferation regulation of FUBP1. Conclusions. Our results indicated that FUBP1 induced the abnormal expression of lncRNAs and the FUBP1-lncRNAs coexpression network in HCC cells, which could provide theoretical and experimental basis for FUBP1-lncRNAs network involved in HCC development.

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