Jianpeng Liu^*, Wei Li^†, Shunshun Liu^*, Xu Zheng^*, Lin Shi^*, Weitao Zhang^*, Hongfa Yang^*

Oncology Research, Vol.25, No.2, pp. 225-232, 2017, DOI:10.3727/096504016X14732772150587

Abstract Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix-related protein, has been found to be upregulated in many solid tumors and contributes to tumorigenesis. We found that CTHRC1 is overexpressed in glioblastoma tissues and cells. By using the technique of RNA interference, the expression of CTHRC1 in the human glioblastoma U-87MG cell line was downregulated, and the proliferation and migration of U-87MG cells were examined. The results showed that the knockdown of CTHRC1 exerts inhibitory effects on the proliferation and migration ability of U-87MG cells. Knockdown of CTHRC1 expression in U-87MG cells resulted in More >

Jie Huang^*, Li Guo^†

Oncology Research, Vol.25, No.2, pp. 167-176, 2017, DOI:10.3727/096504016X14732772150307

Abstract Sex-determining region Y (SRY)-box 9 (SOX9) is a member of the SOX transcription factor family. Increasing evidence has reported that SOX9 plays different roles in various types of malignancies. However, the role of SOX9 in papillary thyroid cancer (PTC) is still unclear. The aim of this study was to investigate the role of SOX9 in PTC. Our results showed that SOX9 was upregulated in PTC tissues and cell lines. In addition, knockdown of SOX9 significantly inhibited PTC proliferation, colony formation, migration, and invasion, as well as epithelial–mesenchymal transition (EMT) phenotype in TPC-1 and BCPAP cells. 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 >

Minglei Zhang^*, Dapeng Wang^†, Tongtong Zhu^*, Ruofeng Yin^*

Oncology Research, Vol.25, No.1, pp. 83-91, 2017, DOI:10.3727/096504016X14719078133447

Abstract RASSF4, a member of the RASSF family, is broadly expressed in normal tissues but often inactivated in human cancers. Despite various studies on RASSF4, its role in osteosarcoma remains unclear. Therefore, in this study, we investigated the effects of RASSF4 expression on osteosarcoma cells and explored the underlying mechanism. The results of our study showed that RASSF4 was lowly expressed in osteosarcoma tissues and cells. RASSF4 overexpression significantly inhibited proliferation, migration, and invasion as well as the EMT process in osteosarcoma cells. Meanwhile, we found that RASSF4 overexpression markedly decreased the protein expression of β-catenin, More >

Yao Shi^*, Xiaoke Sun^†, Xiafen He^‡

Oncology Research, Vol.25, No.1, pp. 11-18, 2017, DOI:10.3727/096504016X14685034103833

Abstract Aristaless-like homeobox-4 (ALX4), a member of the Aristaless-like homeobox family, has been found to be involved in tumor cell proliferation, migration, and invasion. However, the role of ALX4 in hepatocellular carcinoma (HCC) remains largely unclear. Therefore, in this study we investigated the effects of ALX4 on HCC. The study results indicated that the expression of ALX4 was downregulated in HCC tissues and cell lines. Furthermore, we demonstrated that overexpression of ALX4 inhibited the proliferation, invasion, and epithelial–mesenchymal transition (EMT) in HCC cells. We also found that ALX4 had an inhibitory effect on the sonic hedgehog More >

Yanhua Li^*1, Xia Chen^†1, Hong Lu^*

Oncology Research, Vol.24, No.6, pp. 511-519, 2016, DOI:10.3727/096504016X14719078133483

Abstract The gene solute carrier family 34 (sodium phosphate), member 2 (SLC34A2), is a member of the SLC34 family. Increasing evidence suggests that SLC34A2 is involved in the development of many human carcinomas. However, its role in hepatocellular carcinoma (HCC) is still unclear. Therefore, in this study we investigated the role of SLC34A2 in HCC and explored the underlying mechanism. We found that the expression of SLC34A2 is upregulated in HCC cell lines. Knockdown of SLC34A2 obviously inhibited HCC cell proliferation, migration/invasion, and the epithelial–mesenchymal transition (EMT) phenotype. Furthermore, knockdown of SLC34A2 significantly inhibited the expression More >

Xuexin Gao^*, Xuezhen Gao^†, Chao Li^*, Yukun Zhang^*, Lei Gao^‡

Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G₀/G₁ phase in More >

Liu Feng^*†, Wang Wei^*, Zhang Heng^†, Han Yantao^‡, Wang Chunbo^‡

Oncology Research, Vol.24, No.5, pp. 315-325, 2016, DOI:10.3727/096504016X14666990347590

Abstract REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, More >

Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, Yuan-wei Li

Oncology Research, Vol.24, No.5, pp. 305-313, 2016, DOI:10.3727/096504016X14666990347437

Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer 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 >