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  • Open Access

    ARTICLE

    Targeting LncRNA LLNLR-299G3.1 with antisense oligonucleotide inhibits malignancy of esophageal squamous cell carcinoma cells in vitro and in vivo

    LI TIAN1,#, YONGYI HUANG1,#, BAOZHEN ZHANG2,#, YI SONG1,#, LIN YANG3, QIANQIAN CHEN1, ZHENG WANG3, YILING WANG1, QIHAN HE1, WENHAN YANG1, SHUYONG YU4, TIANYU LU5, ZICHEN LIU1, KAIPING GAO1,*, XIUJUN FAN2,*, JIAN SONG4,*, RIHONG ZHAI1,*

    Oncology Research, Vol.31, No.4, pp. 463-479, 2023, DOI:10.32604/or.2023.028791 - 25 June 2023

    Abstract Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of cancers, including esophageal squamous cell carcinoma (ESCC). However, the mechanisms of lncRNAs in ESCC are still incompletely understood and therapeutic attempts for in vivo targeting cancer-associated lncRNA remain a challenge. By RNA-sequencing analysis, we identified that LLNLR-299G3.1 was a novel ESCC-associated lncRNA. LLNLR-299G3.1 was up-regulated in ESCC tissues and cells and promoted ESCC cell proliferation and invasion. Silencing of LLNLR-299G3.1 with ASO (antisense oligonucleotide) resulted in opposite effects. Mechanistically, LLNLR-299G3.1 bound to cancer-associated RNA binding proteins and regulated the expression… More >

  • Open Access

    ARTICLE

    Overexpression of the Long Noncoding RNA FOXD2-AS1 Promotes Cisplatin Resistance in Esophageal Squamous Cell Carcinoma Through the miR-195/Akt/mTOR Axis

    Huasong Liu*1, Jun Zhang*1, Xiangyu Luo*, Min Zeng*, Liqiang Xu*, Qunxian Zhang*, Hua Liu*, Jialong Guo*, Lanlan Xu

    Oncology Research, Vol.28, No.1, pp. 65-73, 2020, DOI:10.3727/096504019X15656904013079

    Abstract Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) mediate the development of esophageal squamous cell carcinoma (ESCC) via various pathophysiological pathways. This study explored the impact of the lncRNA FOXD2-AS1 on cisplatin resistance in ESCC and its possible mechanisms. Upregulation of FOXD2-AS was detected in patients with ESCC and ESCC cells that are resistant to cisplatin. In an in vitro assay, knockdown of FOXD2-AS1 noticeably inhibited cell invasion and growth, triggered cell death, and repressed the stimulation of the Akt/mTOR axis in cisplatin-resistant ESCC cells (TE-1/DDP). Conversely, the overexpression of FOXD2-AS1 remarkably increased cell More >

  • Open Access

    ARTICLE

    Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells

    Jin Zhang, Danjie Zhang, Liangzhang Sun

    Oncology Research, Vol.25, No.2, pp. 249-257, 2017, DOI:10.3727/096504016X693164

    Abstract Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown. In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice. Downregulation of USP14 also suppressed the migration/invasion in ESCC More >

  • Open Access

    ARTICLE

    miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2

    Xiangrui Meng*1, Xiaoqi Chen†1, Peng Lu, Wang Ma*, Dongli Yue*, Lijie Song*, Qingxia Fan*

    Oncology Research, Vol.25, No.2, pp. 215-223, 2017, DOI:10.3727/096504016X14732772150541

    Abstract Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202… More >

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