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Xinjun Wang - One of the best experts on this subject based on the ideXlab platform.

  • lncRNA KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the miR‑375/YAP pathway.
    International journal of molecular medicine, 2020
    Co-Authors: Panfeng Ding, Bo Liang, Jixin Shou, Xinjun Wang
    Abstract:

    The long non‑coding RNA KCNQ1OT1 is generally recognized as an oncogenic molecule in several human malignant tumors. However, to the best of our knowledge, the role of KCNQ1OT1 in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQ1OT1 in human glioma cell lines and its mechanisms. The glioma cell lines U251 and U87‑MG were used as cell models. Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription‑quantitative PCR and western blotting were used to investigate the expression profiles of key molecules. Migration and invasion assays were conducted to reveal the biological features of glioma cells. The results indicated that KCNQ1OT1 was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis. Additionally, knockdown of KCNQ1OT1 in U251 and U87‑MG cells inhibited cell proliferation, migration and invasion, but had no effect on apoptosis. The effects of KCNQ1OT1 on migration and invasion were partially attributed to enhanced Yes‑associated protein (YAP) expression levels and epithelial‑mesenchymal transition (EMT) signaling. Furthermore, microRNA (miR)‑375 functioned as a link between KCNQ1OT1 and YAP in regulating cell proliferation. Finally, the KCNQ1OT1/miR‑375/YAP axis modulated cell proliferation and cell fate by affecting the modulated YAP‑mediated EMT signaling. In conclusion, the KCNQ1OT1/miR‑375/YAP axis modulated migration and invasion of glioma cells by affecting EMT signaling; thus, targeting KCNQ1OT1 may represent a promising strategy in glioma therapeutics.

  • lncrna KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the mir 375 yap pathway
    International Journal of Molecular Medicine, 2020
    Co-Authors: Panfeng Ding, Bo Liang, Jixin Shou, Xinjun Wang
    Abstract:

    The long non‑coding RNA KCNQ1OT1 is generally recognized as an oncogenic molecule in several human malignant tumors. However, to the best of our knowledge, the role of KCNQ1OT1 in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQ1OT1 in human glioma cell lines and its mechanisms. The glioma cell lines U251 and U87‑MG were used as cell models. Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription‑quantitative PCR and western blotting were used to investigate the expression profiles of key molecules. Migration and invasion assays were conducted to reveal the biological features of glioma cells. The results indicated that KCNQ1OT1 was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis. Additionally, knockdown of KCNQ1OT1 in U251 and U87‑MG cells inhibited cell proliferation, migration and invasion, but had no effect on apoptosis. The effects of KCNQ1OT1 on migration and invasion were partially attributed to enhanced Yes‑associated protein (YAP) expression levels and epithelial‑mesenchymal transition (EMT) signaling. Furthermore, microRNA (miR)‑375 functioned as a link between KCNQ1OT1 and YAP in regulating cell proliferation. Finally, the KCNQ1OT1/miR‑375/YAP axis modulated cell proliferation and cell fate by affecting the modulated YAP‑mediated EMT signaling. In conclusion, the KCNQ1OT1/miR‑375/YAP axis modulated migration and invasion of glioma cells by affecting EMT signaling; thus, targeting KCNQ1OT1 may represent a promising strategy in glioma therapeutics.

Xiaoping Qian - One of the best experts on this subject based on the ideXlab platform.

  • KCNQ1OT1/miR-217/ZEB1 feedback loop facilitates cell migration and epithelial-mesenchymal transition in colorectal cancer
    Cancer biology & therapy, 2019
    Co-Authors: Yinzhu Bian, Guangyi Gao, Qun Zhang, Hanqing Qian, Ninghua Yao, Jing Qian, Baorui Liu, Xiaoping Qian
    Abstract:

    Long noncoding RNAs are widely acknowledged as a group of regulatory factors in various diseases, especially in cancers. KCNQ1 overlapping transcript 1 (KCNQ1OT1) has been reported as oncogene in human cancers. However, the role of KCNQ1OT1 in colorectal cancer (CRC) has not been fully explained. Based on the database analysis, KCNQ1OT1 was highly expressed in CRC samples and predicted the poor prognosis for CRC patients. Functional experiments revealed that KCNQ1OT1 knockdown negatively affected the proliferation, migration and epithelial-mesenchymal transition (EMT) in CRC cells. Moreover, we identified the cytoplasmic localization of KCNQ1OT1 in CRC cells, indicating the post-transcriptional regulation of KCNQ1OT1 on gene expression. Mechanism experiments including RNA Immunoprecipitation (RIP) assay and dual luciferase reporter assays verified that KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) in CRC by sponging microRNA-217 (miR-217) to up-regulate the expression of zinc finger E-box binding homeobox 1 (ZEB1). Further mechanism investigation revealed that ZEB1 enhanced the transcription activity of KCNQ1OT1 by acting as a transcription activator. Finally, rescue assays were designed to demonstrate the effect of KCNQ1OT1-miR-217-ZEB1 feedback loop on proliferation, migration, and EMT of CRC cells. In brief, our research findings revealed that ZEB1-induced upregulation of KCNQ1OT1 improved the proliferation, migration and EMT formation of CRC cells via regulation of miR-217/ZEB1 axis.

  • KCNQ1OT1 mir 217 zeb1 feedback loop facilitates cell migration and epithelial mesenchymal transition in colorectal cancer
    Cancer Biology & Therapy, 2019
    Co-Authors: Yinzhu Bian, Guangyi Gao, Qun Zhang, Hanqing Qian, Ninghua Yao, Jing Qian, Baorui Liu, Xiaoping Qian
    Abstract:

    Long noncoding RNAs are widely acknowledged as a group of regulatory factors in various diseases, especially in cancers. KCNQ1 overlapping transcript 1 (KCNQ1OT1) has been reported as oncogene in human cancers. However, the role of KCNQ1OT1 in colorectal cancer (CRC) has not been fully explained. Based on the database analysis, KCNQ1OT1 was highly expressed in CRC samples and predicted the poor prognosis for CRC patients. Functional experiments revealed that KCNQ1OT1 knockdown negatively affected the proliferation, migration and epithelial-mesenchymal transition (EMT) in CRC cells. Moreover, we identified the cytoplasmic localization of KCNQ1OT1 in CRC cells, indicating the post-transcriptional regulation of KCNQ1OT1 on gene expression. Mechanism experiments including RNA Immunoprecipitation (RIP) assay and dual luciferase reporter assays verified that KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) in CRC by sponging microRNA-217 (miR-217) to up-regulate the expression of zinc finger E-box binding homeobox 1 (ZEB1). Further mechanism investigation revealed that ZEB1 enhanced the transcription activity of KCNQ1OT1 by acting as a transcription activator. Finally, rescue assays were designed to demonstrate the effect of KCNQ1OT1-miR-217-ZEB1 feedback loop on proliferation, migration, and EMT of CRC cells. In brief, our research findings revealed that ZEB1-induced upregulation of KCNQ1OT1 improved the proliferation, migration and EMT formation of CRC cells via regulation of miR-217/ZEB1 axis.

Xiaojun Yan - One of the best experts on this subject based on the ideXlab platform.

  • long non coding rna KCNQ1OT1 promotes nasopharyngeal carcinoma cell cisplatin resistance via the mir 454 usp47 axis
    International Journal of Molecular Medicine, 2021
    Co-Authors: Feng Yuan, Zhiping Lou, Zhifeng Zhou, Xiaojun Yan
    Abstract:

    Long non‑coding RNAs serve an essential role in drug resistance in various types of cancer, including lung, breast and bladder cancer. The present study aimed to investigate whether KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) was associated with cisplatin (DDP) resistance in nasopharyngeal carcinoma (NPC). KCNQ1OT1, microRNA (miR)‑454 and ubiquitin specific peptidase 47 (USP47) expression levels were measured via reverse transcription‑quantitative PCR. 5‑8F/DDP and SUNE‑1/DDP cell viability and chemosensitivity were assessed by performing Cell Counting Kit‑8 assays. Colony forming and Transwell assays were conducted to assess the effect of the KCNQ1OT1/miR‑454/USP47 axis on DDP resistance in NPC cells. The association between miR‑454 and KCNQ1OT1 or USP47 was verified via bioinformatics analysis, dual‑luciferase reporter assays and RIP assays. KCNQ1OT1 and USP47 expression levels were significantly upregulated, whereas miR‑454 expression levels were significantly downregulated in DDP‑resistant NPC cells compared with parental NPC cells. KCNQ1OT1 knockdown promoted chemosensitivity in DDP‑resistant NPC cells (5‑8F/DDP and SUNE‑1/DDP), as indicated by significantly decreased cell proliferation, migration and invasion in the short hairpin RNA (sh)KCNQ1OT1 group compared with the sh‑negative control (NC) group. Moreover, miR‑454 was identified as a target of KCNQ1OT1. KCNQ1OT1 overexpression significantly reversed miR‑454 overexpression‑mediated effects on NPC cell viability and DDP resistance. Furthermore, the results indicated that miR‑454 directly targeted USP47. Compared with the shNC group, USP47 knockdown significantly suppressed NPC cell viability and DDP resistance, which was significantly reversed by co‑transfection with miR‑454 inhibitor. Furthermore, compared with the shNC group, KCNQ1OT1 knockdown significantly downregulated USP47 expression, which was significantly counteracted by miR‑454 knockdown. Collectively, the results of the present study indicated that KCNQ1OT1 enhanced DDP resistance in NPC cells via the miR‑454/USP47 axis, suggesting a potential therapeutic target for patients with DDP‑resistant NPC.

  • Long non‑coding RNA KCNQ1OT1 promotes nasopharyngeal carcinoma cell cisplatin resistance via the miR‑454/USP47 axis.
    International journal of molecular medicine, 2021
    Co-Authors: Feng Yuan, Zhiping Lou, Zhifeng Zhou, Xiaojun Yan
    Abstract:

    Long non‑coding RNAs serve an essential role in drug resistance in various types of cancer, including lung, breast and bladder cancer. The present study aimed to investigate whether KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) was associated with cisplatin (DDP) resistance in nasopharyngeal carcinoma (NPC). KCNQ1OT1, microRNA (miR)‑454 and ubiquitin specific peptidase 47 (USP47) expression levels were measured via reverse transcription‑quantitative PCR. 5‑8F/DDP and SUNE‑1/DDP cell viability and chemosensitivity were assessed by performing Cell Counting Kit‑8 assays. Colony forming and Transwell assays were conducted to assess the effect of the KCNQ1OT1/miR‑454/USP47 axis on DDP resistance in NPC cells. The association between miR‑454 and KCNQ1OT1 or USP47 was verified via bioinformatics analysis, dual‑luciferase reporter assays and RIP assays. KCNQ1OT1 and USP47 expression levels were significantly upregulated, whereas miR‑454 expression levels were significantly downregulated in DDP‑resistant NPC cells compared with parental NPC cells. KCNQ1OT1 knockdown promoted chemosensitivity in DDP‑resistant NPC cells (5‑8F/DDP and SUNE‑1/DDP), as indicated by significantly decreased cell proliferation, migration and invasion in the short hairpin RNA (sh)KCNQ1OT1 group compared with the sh‑negative control (NC) group. Moreover, miR‑454 was identified as a target of KCNQ1OT1. KCNQ1OT1 overexpression significantly reversed miR‑454 overexpression‑mediated effects on NPC cell viability and DDP resistance. Furthermore, the results indicated that miR‑454 directly targeted USP47. Compared with the shNC group, USP47 knockdown significantly suppressed NPC cell viability and DDP resistance, which was significantly reversed by co‑transfection with miR‑454 inhibitor. Furthermore, compared with the shNC group, KCNQ1OT1 knockdown significantly downregulated USP47 expression, which was significantly counteracted by miR‑454 knockdown. Collectively, the results of the present study indicated that KCNQ1OT1 enhanced DDP resistance in NPC cells via the miR‑454/USP47 axis, suggesting a potential therapeutic target for patients with DDP‑resistant NPC.

Jingying Zhou - One of the best experts on this subject based on the ideXlab platform.

  • Long noncoding RNA KCNQ1OT1 contributes to tumor growth and activates Wnt/β‑catenin signaling in osteosarcoma by targeting the miR‑3666/KLF7 axis.
    International journal of molecular medicine, 2020
    Co-Authors: Aijun Huang, Song Jin, Weidong Han, Yiming Wang, Zengrong Wang, Kun Lin, Qingbao Zou, Jingying Zhou
    Abstract:

    Osteosarcoma (OS) is a type of primary malignant cancer occurring in the bone and poses a threat to the lives of children and young adults. Long non‑coding RNAs (lncRNAs) have been certified to play important roles in various human malignant tumors, including OS. lncRNA KCNQ1OT1 has been investigated in certain types of cancer; however, its role and molecular mechanisms in OS remain to be determined. In the present study, a high KCNQ1OT1 expression was detected in human OS tissues and cell lines. Moreover, patients with OS with a high expression of KCNQ1OT1 presented a worse prognosis. Loss‑of‑function assays demonstrated that KCNQ1OT1 silencing suppressed cell proliferative, migratory and invasive abilities in OS. Importantly, the knockdown of KCNQ1OT1 suppressed the Wnt/β‑catenin signaling pathway in OS. In vivo assays displayed the inhibitory role of the silencing of KCNQ1OT1 in OS tumor growth. As regards the underlying mechanisms, KCNQ1OT1 could sponge miR‑3666, and its expression was negatively associated with that of miR‑3666 in OS tissues. Thereafter, Kruppel‑like factor 7 (KLF7), upregulated in OS tissues and cells, was discerned as a target gene of miR‑3666. Furthermore, KLF7 expression negatively correlated with miR‑3666 expression, whereas it positively correlated with KCNQ1OT1 expression. A rescue assay delineated that the overexpression of KLF7 counteracted the KCNQ1OT1 knockdown‑induced suppression of OS cell proliferation, migration, invasion and Wnt/β‑catenin signaling. Collectively, the present study demonstrates that KCNQ1OT1 facilitates OS progression and activates Wnt/β‑catenin signaling by targeting the miR‑3666/KLF7 axis.

  • long noncoding rna KCNQ1OT1 contributes to tumor growth and activates wnt β catenin signaling in osteosarcoma by targeting the mir 3666 klf7 axis
    International Journal of Molecular Medicine, 2020
    Co-Authors: Aijun Huang, Song Jin, Weidong Han, Yiming Wang, Zengrong Wang, Kun Lin, Qingbao Zou, Jingying Zhou, Liping Chen
    Abstract:

    Osteosarcoma (OS) is a type of primary malignant cancer occurring in the bone and poses a threat to the lives of children and young adults. Long non‑coding RNAs (lncRNAs) have been certified to play important roles in various human malignant tumors, including OS. lncRNA KCNQ1OT1 has been investigated in certain types of cancer; however, its role and molecular mechanisms in OS remain to be determined. In the present study, a high KCNQ1OT1 expression was detected in human OS tissues and cell lines. Moreover, patients with OS with a high expression of KCNQ1OT1 presented a worse prognosis. Loss‑of‑function assays demonstrated that KCNQ1OT1 silencing suppressed cell proliferative, migratory and invasive abilities in OS. Importantly, the knockdown of KCNQ1OT1 suppressed the Wnt/β‑catenin signaling pathway in OS. In vivo assays displayed the inhibitory role of the silencing of KCNQ1OT1 in OS tumor growth. As regards the underlying mechanisms, KCNQ1OT1 could sponge miR‑3666, and its expression was negatively associated with that of miR‑3666 in OS tissues. Thereafter, Kruppel‑like factor 7 (KLF7), upregulated in OS tissues and cells, was discerned as a target gene of miR‑3666. Furthermore, KLF7 expression negatively correlated with miR‑3666 expression, whereas it positively correlated with KCNQ1OT1 expression. A rescue assay delineated that the overexpression of KLF7 counteracted the KCNQ1OT1 knockdown‑induced suppression of OS cell proliferation, migration, invasion and Wnt/β‑catenin signaling. Collectively, the present study demonstrates that KCNQ1OT1 facilitates OS progression and activates Wnt/β‑catenin signaling by targeting the miR‑3666/KLF7 axis.

Aijun Huang - One of the best experts on this subject based on the ideXlab platform.

  • Long noncoding RNA KCNQ1OT1 contributes to tumor growth and activates Wnt/β‑catenin signaling in osteosarcoma by targeting the miR‑3666/KLF7 axis.
    International journal of molecular medicine, 2020
    Co-Authors: Aijun Huang, Song Jin, Weidong Han, Yiming Wang, Zengrong Wang, Kun Lin, Qingbao Zou, Jingying Zhou
    Abstract:

    Osteosarcoma (OS) is a type of primary malignant cancer occurring in the bone and poses a threat to the lives of children and young adults. Long non‑coding RNAs (lncRNAs) have been certified to play important roles in various human malignant tumors, including OS. lncRNA KCNQ1OT1 has been investigated in certain types of cancer; however, its role and molecular mechanisms in OS remain to be determined. In the present study, a high KCNQ1OT1 expression was detected in human OS tissues and cell lines. Moreover, patients with OS with a high expression of KCNQ1OT1 presented a worse prognosis. Loss‑of‑function assays demonstrated that KCNQ1OT1 silencing suppressed cell proliferative, migratory and invasive abilities in OS. Importantly, the knockdown of KCNQ1OT1 suppressed the Wnt/β‑catenin signaling pathway in OS. In vivo assays displayed the inhibitory role of the silencing of KCNQ1OT1 in OS tumor growth. As regards the underlying mechanisms, KCNQ1OT1 could sponge miR‑3666, and its expression was negatively associated with that of miR‑3666 in OS tissues. Thereafter, Kruppel‑like factor 7 (KLF7), upregulated in OS tissues and cells, was discerned as a target gene of miR‑3666. Furthermore, KLF7 expression negatively correlated with miR‑3666 expression, whereas it positively correlated with KCNQ1OT1 expression. A rescue assay delineated that the overexpression of KLF7 counteracted the KCNQ1OT1 knockdown‑induced suppression of OS cell proliferation, migration, invasion and Wnt/β‑catenin signaling. Collectively, the present study demonstrates that KCNQ1OT1 facilitates OS progression and activates Wnt/β‑catenin signaling by targeting the miR‑3666/KLF7 axis.

  • long noncoding rna KCNQ1OT1 contributes to tumor growth and activates wnt β catenin signaling in osteosarcoma by targeting the mir 3666 klf7 axis
    International Journal of Molecular Medicine, 2020
    Co-Authors: Aijun Huang, Song Jin, Weidong Han, Yiming Wang, Zengrong Wang, Kun Lin, Qingbao Zou, Jingying Zhou, Liping Chen
    Abstract:

    Osteosarcoma (OS) is a type of primary malignant cancer occurring in the bone and poses a threat to the lives of children and young adults. Long non‑coding RNAs (lncRNAs) have been certified to play important roles in various human malignant tumors, including OS. lncRNA KCNQ1OT1 has been investigated in certain types of cancer; however, its role and molecular mechanisms in OS remain to be determined. In the present study, a high KCNQ1OT1 expression was detected in human OS tissues and cell lines. Moreover, patients with OS with a high expression of KCNQ1OT1 presented a worse prognosis. Loss‑of‑function assays demonstrated that KCNQ1OT1 silencing suppressed cell proliferative, migratory and invasive abilities in OS. Importantly, the knockdown of KCNQ1OT1 suppressed the Wnt/β‑catenin signaling pathway in OS. In vivo assays displayed the inhibitory role of the silencing of KCNQ1OT1 in OS tumor growth. As regards the underlying mechanisms, KCNQ1OT1 could sponge miR‑3666, and its expression was negatively associated with that of miR‑3666 in OS tissues. Thereafter, Kruppel‑like factor 7 (KLF7), upregulated in OS tissues and cells, was discerned as a target gene of miR‑3666. Furthermore, KLF7 expression negatively correlated with miR‑3666 expression, whereas it positively correlated with KCNQ1OT1 expression. A rescue assay delineated that the overexpression of KLF7 counteracted the KCNQ1OT1 knockdown‑induced suppression of OS cell proliferation, migration, invasion and Wnt/β‑catenin signaling. Collectively, the present study demonstrates that KCNQ1OT1 facilitates OS progression and activates Wnt/β‑catenin signaling by targeting the miR‑3666/KLF7 axis.