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Search Results (16)
  • Open Access

    ARTICLE

    Knockdown of Collagen Triple Helix Repeat Containing-1 Inhibits the Proliferation and Epithelial-to-Mesenchymal Transition in Renal Cell Carcinoma Cells

    Xue-fei Jin, Hai Li, Shi Zong, Hong-yan Li

    Oncology Research, Vol.24, No.6, pp. 477-485, 2016, DOI:10.3727/096504016X14685034103716

    Abstract Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of More >

  • Open Access

    ARTICLE

    TIPE2 Inhibits Hypoxia-Induced Wnt/β-Catenin Pathway Activation and EMT in Glioma Cells

    Zhi-jun Liu*1, Hong-lin Liu*1, Hai-cun Zhou, Gui-cong Wang*

    Oncology Research, Vol.24, No.4, pp. 255-261, 2016, DOI:10.3727/096504016X14666990347356

    Abstract Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-α-induced protein 8 (TNFAIP8, TIPE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was More >

  • Open Access

    ARTICLE

    IGF-I Induces Epithelial-to-Mesenchymal Transition via the IGF-IR–Src– MicroRNA-30a–E-Cadherin Pathway in Nasopharyngeal Carcinoma Cells

    Ruoyu Wang*†, Heming Li, Xuefen Guo, Zhe Wang, Shanshan Liang, Chengxue Dang*

    Oncology Research, Vol.24, No.4, pp. 225-231, 2016, DOI:10.3727/096504016X14648701447931

    Abstract Recurrence and distant metastasis are the most common cause of therapeutic failure in nasopharyngeal carcinoma (NPC) patients. Insulin-like growth factor I (IGF-I) can induce epithelial-to-mesenchymal transition (EMT) in many epithelial tumors; however, whether IGF-I can enhance NPC metastasis by EMT and the mechanisms remain unclear. Herein, we have identified that IGF-I could induce EMT and enhance migration ability in NPC cell lines. Furthermore, both Src inhibitor and microRNA-30a (miR-30a) inhibitor reversed IGF-I-induced EMT, suggesting the involvement of an IGF-IR–Src–miR-30a–E-cadherin pathway in IGF-Iinduced EMT in NPC cell lines. Overall, the results of the present study may More >

  • Open Access

    ARTICLE

    Knockdown of PFTAIRE Protein Kinase 1 (PFTK1) Inhibits Proliferation, Invasion, and EMT in Colon Cancer Cells

    Jiankang Zhu, Chongzhong Liu, Fengyue Liu, Yadong Wang, Min Zhu

    Oncology Research, Vol.24, No.3, pp. 137-144, 2016, DOI:10.3727/096504016X14611963142218

    Abstract PFTK1 is a member of the cyclin-dependent kinase (CDK) family and is upregulated in many types of tumors. However, its expression and role in colon cancer remain unclear. In this study, we aimed to investigate the expression and function of PFTK1 in colon cancer. Our results showed that PFTK1 was highly expressed in colon cancer cell lines. The in vitro experiments demonstrated that knockdown of PFTK1 inhibited the proliferation, migration, and invasion of colon cancer cells as well as the epithelial-to-mesenchymal transition (EMT) progress. Furthermore, knockdown of PFTK1 suppressed the expression of Shh as well More >

  • Open Access

    ARTICLE

    Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Lung Cancer Cells and Inhibits Regulating Epithelial-to-Mesenchymal Transition

    Shenggang Liu*, Hongzhong Yang, Ying Chen, Baimei He§, Qiong Chen§

    Oncology Research, Vol.24, No.2, pp. 81-87, 2016, DOI:10.3727/096504016X14597766487717

    Abstract In order to improve therapeutic efficacy, it is a current emergency to better know the mechanisms underlying cisplatin resistance in lung cancer cells. In this study, we aim to investigate the role of Krüppel-like factor 4 (KLF4) in cisplatin-resistant lung cancer cells. We developed cisplatin-resistant lung cancer cell line A549/ DDP, and then a battery of experiments was used to analyze the effects of KLF4 in cisplatin resistance of lung cancer. We found that KLF4 was significantly downregulated in cisplatin-resistant A549 cells and forced KLF4 expression inhibited cell growth and induced apoptosis. Further, we found More >

  • Open Access

    ARTICLE

    Upregulation of CD147 Promotes Metastasis of Cholangiocarcinoma by Modulating the Epithelial-to-Mesenchymal Transitional Process

    Paweena Dana*†‡, Ryusho Kariya, KulthidaVaeteewoottacharn*†, Kanlayanee Sawanyawisuth*†, Wunchana Seubwai†§, Kouki Matsuda, Seiji Okada, Sopit Wongkham*†

    Oncology Research, Vol.25, No.7, pp. 1047-1059, 2017, DOI:10.3727/096504016X14813899000565

    Abstract CD147 is a transmembrane protein that can induce the expression and activity of matrix metalloproteinases (MMPs). Expression of CD147 has been shown to potentiate cell migration, invasion, and metastasis of cancer. In this study, the critical role of CD147 in metastasis was elucidated using CD147-overexpressing cholangiocarcinoma (CCA) cells in vitro and in vivo. The molecular mechanism, demonstrated herein, supported the hypothesis that metastasis increased in CD147-overexpressing cells. Five CD147-overexpressing clones (Ex-CD147) were established from a low CD147-expressing CCA cell line, KKU-055, using lentivirus containing pReceiver-Lenti-CD147. The metastatic capability was determined using the tail vein injection… More >

  • Open Access

    ARTICLE

    CDGSH Iron Sulfur Domain 2 Activates Proliferation and EMT of Pancreatic Cancer Cells via Wnt/β-Catenin Pathway and Has Prognostic Value in Human Pancreatic Cancer

    Yang Yang, Yuan-song Bai, Qing Wang

    Oncology Research, Vol.25, No.4, pp. 605-615, 2017, DOI:10.3727/096504016X14767450526417

    Abstract Recently, increasing evidence has shown that CDGSH iron sulfur domain 2 (CISD2) is involved in the initiation and metastasis of several cancers. However, the evidence of its potential role in pancreatic cancer is still lacking. In our present study, CISD2 was found to be increased in pancreatic cancer samples and multiple cell lines. Moreover, statistical analysis revealed that a high level of CISD2 was related to advanced clinical stage, advanced T-stage, positive vascular invasion, positive distant metastasis, and larger tumor size. In addition, multivariate analysis suggests that CISD2 was an independent prognostic factor in pancreatic… More >

  • Open Access

    ARTICLE

    Isolation and Characterization of Fast-Migrating Human Glioma Cells in the Progression of Malignant Gliomas

    Vivian Adamski*, Anne Dorothée Schmitt*, Charlotte Flüh*, Michael Synowitz*, Kirsten Hattermann†1, Janka Held-Feindt*1

    Oncology Research, Vol.25, No.3, pp. 341-353, 2017, DOI:10.3727/096504016X14737243054982

    Abstract Gliomas are the most common primary brain tumors. The most malignant form, the glioblastoma multiforme (GBM; WHO IV), is characterized by an invasive phenotype, which enables the tumor cells to infiltrate into adjacent brain tissue. When investigating GBM migration and invasion properties in vitro, in most cases GBM cell lines were analyzed. Comprehensive investigations focusing on progression-dependent characteristics of migration processes using fresh human glioma samples of different malignancy grades do not exist. Thus, we isolated fast-migrating tumor cells from fresh human glioma samples of different malignancy grades (astrocytomas WHO grade II, grade III, GBM,… More >

  • Open Access

    ARTICLE

    Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF-β-Induced EMT in Bladder Carcinoma UMUC3 Cells

    Xuan Liang*, Qun-Li Men, Yong-wei Li, He-Cheng Li§, Tie Chong§, Zhao-lun Li§

    Oncology Research, Vol.25, No.1, pp. 99-105, 2017, DOI:10.3727/096504016X14719078133609

    Abstract Armadillo repeat-containing protein 8 (ARMc8) is a key factor in regulating cell migration, proliferation, tissue maintenance, and tumorigenesis. However, its role in bladder cancer remains unknown. Thus, in this study we sought to investigate the effect of ARMc8 on the epithelial-to-mesenchymal transition (EMT) progress in bladder cancer cells induced by transforming growth factor-b1 (TGF-β1). Our results found that ARMc8 was highly expressed in bladder cancer cell lines. ARMc8 silencing inhibited the TGF-β1-induced migration and invasion and suppressed the EMT progress in bladder cancer cells. Furthermore, ARMc8 silencing inhibited the TGF-β1-induced expression of β-catenin, cyclin D1, More >

  • Open Access

    ARTICLE

    5-Fluorouracil dose escalation generated desensitized colorectal cancer cells with reduced expression of protein methyltransferases and no epithelial-to-mesenchymal transition potential

    KIMBERLY FENECH1, ISAAC MICALLEF1,2, BYRON BARON1,*

    Oncology Research, Vol.32, No.6, pp. 1047-1061, 2024, DOI:10.32604/or.2024.049173

    Abstract Background: Colorectal cancer (CRC) is one of the most frequently diagnosed cancers. In many cases, the poor prognosis of advanced CRC is associated with resistance to treatment with chemotherapeutic drugs such as 5-Fluorouracil (5-FU). The epithelial-to-mesenchymal transition (EMT) and dysregulation in protein methylation are two mechanisms associated with chemoresistance in many cancers. This study looked into the effect of 5-FU dose escalation on EMT and protein methylation in CRC. Materials and Methods: HCT-116, Caco-2, and DLD-1 CRC cell lines were exposed to dose escalation treatment of 5-FU. The motility and invasive potentials of the cells before… More > Graphic Abstract

    5-Fluorouracil dose escalation generated desensitized colorectal cancer cells with reduced expression of protein methyltransferases and no epithelial-to-mesenchymal transition potential

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