13 results on '"linc01134"'
Search Results
2. Silenced LINC01134 Enhances Oxaliplatin Sensitivity by Facilitating Ferroptosis Through GPX4 in Hepatocarcinoma
- Author
-
Xiaofeng Kang, Yan Huo, Songhao Jia, Fuliang He, Huizi Li, Qing Zhou, Nijia Chang, Donghui Liu, Rongkuan Li, Yi Hu, Ping Zhang, and An Xu
- Subjects
linc01134 ,Nrf2 ,GPx4 ,OXA ,ferroptosis ,HCC cancer ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
PurposeRecently, long noncoding RNA LINC01134 has been shown to reduce cell viability and apoptosis via the antioxidant stress pathway, thereby enhancing OXA resistance in hepatocellular carcinoma. However, the association of LINC01134 with ferroptosis and the underlying molecular mechanisms remain to be elucidated.MethodsBioinformatics analysis was employed to screen lncRNAs positively correlated with GPX4 and poor clinical prognosis. And Western blot and RT-PCR analysis in HCC cells confirmed the effect of LINC01134 on GPX4 expression. In addition, LINC01134 siRNA was transfected in HCC cells to detect the changes in cell viability, ROS, lipid peroxidation, MDA levels and GSH/GSSG levels. CCK-8, colony formation and apoptosis assays were performed to determine the effect of LINC01134 on cell death. The effect of LINC01134 and OXA on Nrf2 transcriptional binding to GPX4 was analyzed using dual luciferase reporter assay and CHIP. The expression of GPX4 and Nrf2 in HCC tissues was detected by FISH and IHC.ResultsLINC01134 is a novel lncRNA positively correlated with GPx4 and associated with poor clinical prognosis. Silenced LINC01134 conferred OXA sensitivity by enhancing total ROS, lipid ROS, MDA levels and decreasing GSH/GSSG ratio. Mechanistically, LINC01134 and OXA could promote Nrf2 recruitment to the GPX4 promoter region to exert transcriptional regulation of GPX4. Clinically, LINC01134 was positively correlated with GPX4 or Nrf2, demonstrating the clinical significance of LINC01134, Nrf2 and GPX4 in OXA resistance of HCC.ConclusionsWe identified LINC01134/Nrf2/GPX4 as a novel and critical axis to regulate HCC growth and progression. Targeting GPX4, knocking down LINC01134 or Nrf2 could be a potential therapeutic strategy for HCC.
- Published
- 2022
- Full Text
- View/download PDF
3. Establishment of a lncRNA-Based Prognostic Gene Signature Associated With Altered Immune Responses in HCC.
- Author
-
Li, Xiawei, Zhang, Zhiqian, Liu, Mingcheng, Fu, Xing, A, Jun, Chen, Guoan, Wu, Shian, and Dong, Jin-Tang
- Subjects
IMMUNE response ,T cells ,B cells ,DENDRITIC cells ,REGRESSION analysis - Abstract
Hepatocellular carcinoma (HCC) is a common malignancy with higher mortality, and means are urgently needed to improve the prognosis. T cell exclusion (TCE) plays a pivotal role in immune evasion, and lncRNAs represent a large group of tumor development and progression modulators. Using the TCGA HCC dataset (n=374), we identified 2752 differentially expressed and 702 TCE-associated lncRNAs, of which 336 were in both groups. As identified using the univariate Cox regression analysis, those associated with overall survival (OS) were subjected to the LASSO-COX regression analysis to develop a prognosis signature. The model, which consisted of 11 lncRNAs and was named 11LNCPS for 11-lncRNA prognosis signature, was validated and performed better than two previous models. In addition to OS and TCE, higher 11LNCPS scores had a significant correlation with reduced infiltrations of CD8+ T cells and dendritic cells (DCs) and decreased infiltrations of Th1, Th2, and pro B cells. As expected, these infiltration alterations were significantly associated with worse OS in HCC. Analysis of published data indicates that HCCs with higher 11LNCPS scores were transcriptomically similar to those that responded better to PDL1 inhibitor. Of the 11LNCPS lncRNAs, LINC01134 and AC116025.2 seem more crucial, as their upregulations affected more immune cell types' infiltrations and were significantly associated with TCE, worse OS, and compromised immune responses in HCC. LncRNAs in the 11LNCPS impacted many cancer-associated biological processes and signaling pathways, particularly those involved in immune function and metabolism. The 11LNCPS should be useful for predicting prognosis and immune responses in HCC. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
4. Establishment of a lncRNA-Based Prognostic Gene Signature Associated With Altered Immune Responses in HCC
- Author
-
Xiawei Li, Zhiqian Zhang, Mingcheng Liu, Xing Fu, Jun A, Guoan Chen, Shian Wu, and Jin-Tang Dong
- Subjects
hepatocellular carcinoma (HCC) ,T cell exclusion ,lncRNA ,prognosis ,LINC01134 ,AC116025.2 ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Hepatocellular carcinoma (HCC) is a common malignancy with higher mortality, and means are urgently needed to improve the prognosis. T cell exclusion (TCE) plays a pivotal role in immune evasion, and lncRNAs represent a large group of tumor development and progression modulators. Using the TCGA HCC dataset (n=374), we identified 2752 differentially expressed and 702 TCE-associated lncRNAs, of which 336 were in both groups. As identified using the univariate Cox regression analysis, those associated with overall survival (OS) were subjected to the LASSO-COX regression analysis to develop a prognosis signature. The model, which consisted of 11 lncRNAs and was named 11LNCPS for 11-lncRNA prognosis signature, was validated and performed better than two previous models. In addition to OS and TCE, higher 11LNCPS scores had a significant correlation with reduced infiltrations of CD8+ T cells and dendritic cells (DCs) and decreased infiltrations of Th1, Th2, and pro B cells. As expected, these infiltration alterations were significantly associated with worse OS in HCC. Analysis of published data indicates that HCCs with higher 11LNCPS scores were transcriptomically similar to those that responded better to PDL1 inhibitor. Of the 11LNCPS lncRNAs, LINC01134 and AC116025.2 seem more crucial, as their upregulations affected more immune cell types’ infiltrations and were significantly associated with TCE, worse OS, and compromised immune responses in HCC. LncRNAs in the 11LNCPS impacted many cancer-associated biological processes and signaling pathways, particularly those involved in immune function and metabolism. The 11LNCPS should be useful for predicting prognosis and immune responses in HCC.
- Published
- 2022
- Full Text
- View/download PDF
5. LncRNA LINC01134 Contributes to Radioresistance in Hepatocellular Carcinoma by Regulating DNA Damage Response via MAPK Signaling Pathway.
- Author
-
Wang, Zhiyi, Wang, Xinxing, Rong, Zhonghou, Dai, Longfei, Qin, Chengkun, Wang, Shikang, and Geng, Wenmao
- Subjects
DNA repair ,LINCRNA ,DNA damage ,SOMATOMEDIN A ,MITOGEN-activated protein kinase kinase ,HEPATOCELLULAR carcinoma ,CELLULAR signal transduction - Abstract
Hepatocellular carcinoma (HCC) is a highly mortal cancer that could be treated by radiotherapy. DNA damage response (DDR) is a vital factor affecting cancer development after radiotherapy. Long non-coding RNAs (lncRNAs) have been revealed to regulate DNA damage response and repair in cancer cells. Nevertheless, the function of long intergenic non-protein coding RNA 1134 (LINC01134) has not been explored in DDR. In this study, we targeted digging into the function of LINC01134 in DDR and exploring the underlying mechanism in HCC cells. RT-qPCR was employed to measure LINC01134 expression, and we found LINC01134 was significantly upregulated in HCC cells. Functional analysis suggested that LINC01134 depletion attenuated radioresistance of HCC cells by facilitating DNA damage. In vivo assays demonstrated LINC01134 depletion hindered HCC tumor growth. Mechanism assays unveiled LINC01134 sequestered microRNA-342-3p (miR-342-3p) and recruited insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) protein to modulate mitogen-activated protein kinase 1 (MAPK1) expression, consequently activating MAPK signaling pathway. Rescue assays validated the LINC01134/miR-342-3p/MAPK1 axis in the radio-resistant HCC cells. In conclusion, LINC01134 might be identified to be a useful biomarker for the therapy of HCC. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
6. Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression
- Author
-
Zhonghou Rong, Zhiyi Wang, Xinxing Wang, Chengkun Qin, and Wenmao Geng
- Subjects
YY1 ,linc01134 ,IGF2BP1 ,Hepatocellular carcinoma ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Revealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet. Materials and methods qRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes. Results YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop. Conclusion Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.
- Published
- 2020
- Full Text
- View/download PDF
7. LncRNA LINC01134 Contributes to Radioresistance in Hepatocellular Carcinoma by Regulating DNA Damage Response via MAPK Signaling Pathway
- Author
-
Zhiyi Wang, Xinxing Wang, Zhonghou Rong, Longfei Dai, Chengkun Qin, Shikang Wang, and Wenmao Geng
- Subjects
DNA damage ,linc01134 ,MiR-342-3p ,IGF2BP2 ,MAPK1 ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Hepatocellular carcinoma (HCC) is a highly mortal cancer that could be treated by radiotherapy. DNA damage response (DDR) is a vital factor affecting cancer development after radiotherapy. Long non-coding RNAs (lncRNAs) have been revealed to regulate DNA damage response and repair in cancer cells. Nevertheless, the function of long intergenic non-protein coding RNA 1134 (LINC01134) has not been explored in DDR. In this study, we targeted digging into the function of LINC01134 in DDR and exploring the underlying mechanism in HCC cells. RT-qPCR was employed to measure LINC01134 expression, and we found LINC01134 was significantly upregulated in HCC cells. Functional analysis suggested that LINC01134 depletion attenuated radioresistance of HCC cells by facilitating DNA damage. In vivo assays demonstrated LINC01134 depletion hindered HCC tumor growth. Mechanism assays unveiled LINC01134 sequestered microRNA-342-3p (miR-342-3p) and recruited insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) protein to modulate mitogen-activated protein kinase 1 (MAPK1) expression, consequently activating MAPK signaling pathway. Rescue assays validated the LINC01134/miR-342-3p/MAPK1 axis in the radio-resistant HCC cells. In conclusion, LINC01134 might be identified to be a useful biomarker for the therapy of HCC.
- Published
- 2022
- Full Text
- View/download PDF
8. LINC01134: a pivotal oncogene with promising predictive maker and therapeutic target in hepatocellular carcinoma.
- Author
-
Yu Y, Wang J, Guo Q, and Luo H
- Abstract
Hepatocellular carcinoma (HCC) represents a leading and fatal malignancy within the gastrointestinal tract. Recent advancements highlight the pivotal role of long non-coding RNAs (lncRNAs) in diverse biological pathways and pathologies, particularly in tumorigenesis. LINC01134, a particular lncRNA, has attracted considerable attention due to its oncogenic potential in hepatoma. Current research underscores LINC01134's potential in augmenting the onset and progression of HCC, with notable implications in drug resistance. This review comprehensively explores the molecular functions and regulatory mechanisms of LINC01134 in HCC, offering a fresh perspective for therapeutic interventions. By delving into LINC01134's multifaceted roles, we aim to foster novel strategies in HCC management., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yu, Wang, Guo and Luo.)
- Published
- 2024
- Full Text
- View/download PDF
9. Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression.
- Author
-
Rong, Zhonghou, Wang, Zhiyi, Wang, Xinxing, Qin, Chengkun, and Geng, Wenmao
- Subjects
- *
SOMATOMEDIN A , *HEPATOCELLULAR carcinoma , *NON-coding RNA - Abstract
Background: Revealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet. Materials and methods: qRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes. Results: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop. Conclusion: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
10. Long intergenic noncoding RNA01134 accelerates hepatocellular carcinoma progression by sponging microRNA-4784 and downregulating structure specific recognition protein 1
- Author
-
Ziming Liang, Qing Yang, Lizhen Dai, Shiyang Zheng, Yan Guo, and Shu-hong Yi
- Subjects
0301 basic medicine ,Carcinoma, Hepatocellular ,Blotting, Western ,Bioengineering ,Biology ,In Vitro Techniques ,medicine.disease_cause ,Applied Microbiology and Biotechnology ,Cell Line ,linc01134 ,03 medical and health sciences ,0302 clinical medicine ,ssrp1 ,Downregulation and upregulation ,microRNA ,medicine ,Humans ,Immunoprecipitation ,neoplasms ,Competing endogenous RNA ,Reverse Transcriptase Polymerase Chain Reaction ,Liver Neoplasms ,RNA ,General Medicine ,hepatocellular carcinoma ,medicine.disease ,Long non-coding RNA ,digestive system diseases ,mir‐4784 ,MicroRNAs ,030104 developmental biology ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Cancer research ,RNA, Long Noncoding ,long noncoding rna ,Structure specific recognition protein 1 ,Carcinogenesis ,TP248.13-248.65 ,Research Article ,Research Paper ,Biotechnology - Abstract
Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC., Graphical Abstract
- Published
- 2020
11. Silenced LINC01134 Enhances Oxaliplatin Sensitivity by Facilitating Ferroptosis Through GPX4 in Hepatocarcinoma.
- Author
-
Kang X, Huo Y, Jia S, He F, Li H, Zhou Q, Chang N, Liu D, Li R, Hu Y, Zhang P, and Xu A
- Abstract
Purpose: Recently, long noncoding RNA LINC01134 has been shown to reduce cell viability and apoptosis via the antioxidant stress pathway, thereby enhancing OXA resistance in hepatocellular carcinoma. However, the association of LINC01134 with ferroptosis and the underlying molecular mechanisms remain to be elucidated., Methods: Bioinformatics analysis was employed to screen lncRNAs positively correlated with GPX4 and poor clinical prognosis. And Western blot and RT-PCR analysis in HCC cells confirmed the effect of LINC01134 on GPX4 expression. In addition, LINC01134 siRNA was transfected in HCC cells to detect the changes in cell viability, ROS, lipid peroxidation, MDA levels and GSH/GSSG levels. CCK-8, colony formation and apoptosis assays were performed to determine the effect of LINC01134 on cell death. The effect of LINC01134 and OXA on Nrf2 transcriptional binding to GPX4 was analyzed using dual luciferase reporter assay and CHIP. The expression of GPX4 and Nrf2 in HCC tissues was detected by FISH and IHC., Results: LINC01134 is a novel lncRNA positively correlated with GPx4 and associated with poor clinical prognosis. Silenced LINC01134 conferred OXA sensitivity by enhancing total ROS, lipid ROS, MDA levels and decreasing GSH/GSSG ratio. Mechanistically, LINC01134 and OXA could promote Nrf2 recruitment to the GPX4 promoter region to exert transcriptional regulation of GPX4. Clinically, LINC01134 was positively correlated with GPX4 or Nrf2, demonstrating the clinical significance of LINC01134, Nrf2 and GPX4 in OXA resistance of HCC., Conclusions: We identified LINC01134/Nrf2/GPX4 as a novel and critical axis to regulate HCC growth and progression. Targeting GPX4, knocking down LINC01134 or Nrf2 could be a potential therapeutic strategy for HCC., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Kang, Huo, Jia, He, Li, Zhou, Chang, Liu, Li, Hu, Zhang and Xu.)
- Published
- 2022
- Full Text
- View/download PDF
12. Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression
- Author
-
Zhonghou Rong, Wenmao Geng, Xinxing Wang, Zhi-Yi Wang, and Cheng-Kun Qin
- Subjects
Cancer Research ,Carcinoma, Hepatocellular ,Carcinogenesis ,Hepatocellular carcinoma ,medicine.medical_treatment ,Mice, Nude ,Cell Cycle Proteins ,medicine.disease_cause ,Transfection ,lcsh:RC254-282 ,YY1 ,Flow cytometry ,linc01134 ,Mice ,Western blot ,Transcription (biology) ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Promoter Regions, Genetic ,Gene knockdown ,Mice, Inbred BALB C ,medicine.diagnostic_test ,IGF2BP1 ,Chemistry ,Growth factor ,Research ,Liver Neoplasms ,RNA ,Hep G2 Cells ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Oncology ,Cancer research ,Disease Progression ,Heterografts ,RNA, Long Noncoding ,Transcription Factors - Abstract
BackgroundRevealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet.Materials and methodsqRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes.ResultsYY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop.ConclusionLinc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.
- Published
- 2019
13. Long intergenic noncoding RNA01134 accelerates hepatocellular carcinoma progression by sponging microRNA-4784 and downregulating structure specific recognition protein 1.
- Author
-
Zheng S, Guo Y, Dai L, Liang Z, Yang Q, and Yi S
- Subjects
- Blotting, Western, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Cell Line, Humans, Immunoprecipitation, In Vitro Techniques, Liver Neoplasms genetics, Liver Neoplasms metabolism, Liver Neoplasms pathology, MicroRNAs genetics, Reverse Transcriptase Polymerase Chain Reaction, MicroRNAs metabolism, RNA, Long Noncoding genetics, RNA, Long Noncoding metabolism
- Abstract
Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC.
- Published
- 2020
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.