Li Dong¹, Tian Bo², Jin Xiaosheng³

Oncology Research, Vol.27, No.1, pp. 9-17, 2019, DOI:10.3727/096504018X15178732625479

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHERS IN OCTOBER 2020. More >

Fan-Chun Meng, Jun-Kai Lin

Oncology Research, Vol.27, No.2, pp. 139-146, 2019, DOI:10.3727/096504018X15185747911701

Abstract Inhibition of tumor metastasis is one of the most important purposes in colorectal cancer (CRC) treatment. This study aimed to explore the effects of liquiritigenin, a flavonoid extracted from the roots of Glycyrrhiza uralensis Fisch, on HCT116 cell proliferation, invasion, and epithelial-to-mesenchymal transition (EMT). We found that liquiritigenin significantly inhibited HCT116 cell proliferation, invasion, and the EMT process, but had no influence on cell apoptosis. Moreover, liquiritigenin remarkably reduced the expression of runt-related transcription factor 2 (Runx2) in HCT116 cells. Overexpression of Runx2 obviously reversed the liquiritigenininduced invasion and EMT inhibition. Furthermore, liquiritigenin inactivated the More >

Xiaofei Ning^*, Cong Wang^†, Meng Zhang^†, Kecheng Wang^*

Oncology Research, Vol.27, No.4, pp. 399-406, 2019, DOI:10.3727/096504018X15179675206495

Abstract Colon cancer is one of the most common cancers in the world. Epithelial-to-mesenchymal transition (EMT) is a crucial step in tumor progression and is also involved in the acquisition of stem cell-like properties. Some miRNAs have been shown to function as either tumor suppressors or oncogenes in colon cancer. Here we investigated the role of miR-147 in the regulation of the stem cell-like traits of colon cancer cells. We observed that miR-147 was downregulated in several colon cancer cell lines, and overexpressed miR-147 decreased the expression of cancer stem cell (CSC) markers OCT4, SOX2, and… More >

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 >

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 >

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 >

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 >

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 >

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 >