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  • Open Access

    ARTICLE

    Inhibition of ERK1/2 Signaling Impairs the Promoting Effects of TGF-β1 on Hepatocellular Carcinoma Cell Invasion and Epithelial–Mesenchymal Transition

    Ling Liu, Nianfeng Li, Qi Zhang, Jixiang Zhou, Ling Lin, Xinxin He

    Oncology Research, Vol.25, No.9, pp. 1607-1616, 2017, DOI:10.3727/096504017X14938093512742

    Abstract Transforming growth factor-b (TGF-β) and ERK signaling have been implicated in various human cancers including hepatocellular carcinoma, but the underlying mechanism remains largely unclear. In this study, we aimed to explore the role of ERK1/2 in the regulation of TGF-β’s promoting and suppressive activities in HCC cells. Our data showed that treatment with TGF-β1 enhanced invasion and epithelial–mesenchymal transition (EMT) in HCC HepG2 cells, accompanied with increased MMP9 production and activation of Smad2/3 and ERK1/2, but inhibited tumor cell proliferation. These effects were eliminated by treatment with SB431542, a TGF-β inhibitor. Afterward, treatment with the… More >

  • Open Access

    ARTICLE

    Inhibition of MMP-2 Expression Enhances the Antitumor Effect of Sorafenib in Hepatocellular Carcinoma by Suppressing the PI3K/AKT/mTOR Pathway

    Wenliang Tan*†1, Sicong Zhu*†1, Jun Cao*†, Lei Zhang*†, Wenda Li*†, Kairui Liu*†, Jinyi Zhong, Changzhen Shang*†, Yajin Chen*†

    Oncology Research, Vol.25, No.9, pp. 1543-1553, 2017, DOI:10.3727/096504017X14886444100783

    Abstract Sorafenib has been globally approved as the standard treatment for patients with advanced hepatocellular carcinoma (HCC). However, the response rate of HCC patients to sorafenib is limited because of tumor recurrence and metastasis. Therefore, seeking combined therapeutic strategies with sorafenib is necessary to improve the antitumor efficiency. Here we demonstrated that expression of MMP-2 is positively correlated with the migration ability of HCC cells. Cells with a higher MMP-2 expression (SK-HEP-1 cells) were less sensitive to sorafenib than those with lower MMP-2 expression (HepG2 cells). Cotreatment of cells with SB-3CT and sorafenib more strongly inhibited… More >

  • Open Access

    ARTICLE

    UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer by Sponging miR-135a

    Xiaobo Zhang*, Feng Gao*, Lei Zhou*, Huaitao Wang*, Gang Shi, Xiaodong Tan*

    Oncology Research, Vol.25, No.9, pp. 1529-1541, 2017, DOI:10.3727/096504017X14888987683152

    Abstract Pancreatic cancer (PC) is a devastating malignant disease with a poor prognosis. This study aimed to investigate the role of urothelial carcinoma associated 1 (UCA1) in the progression of PC. Our results revealed that long noncoding RNA (lncRNA) UCA1 was overexpressed in PC tissues compared with adjacent histologically normal tissues. A downregulated level of UCA1 was also detected in five human PC cell lines (SW1990, BxPC-3, MiaPaCa-2, PANC-1, and CAPAN-1) compared with normal pancreatic duct epithelial HPDE cells. The proliferation of PC cells was inhibited after UCA1 was suppressed by a lentiviral vector. The cell… More >

  • Open Access

    ARTICLE

    Overexpression of T-box Transcription Factor 5 (TBX5) Inhibits Proliferation and Invasion in Non-Small Cell Lung Carcinoma Cells

    Ruoting Ma*†, Yu Yang*, Qiuyun Tu, Ke Hu

    Oncology Research, Vol.25, No.9, pp. 1495-1504, 2017, DOI:10.3727/096504017X14883287513729

    Abstract T-box transcription factor 5 (TBX5), a member of the conserved T-box transcription factor family that functions in organogenesis and embryogenesis, has recently been identified as a critical player in cancer development. The aim of this study was to determine the role of TBX5 in non-small cell lung carcinoma (NSCLC). Immunohistochemistry was used to detect the correlation between levels of TBX5 and clinicopathological features of NSCLC patients in tissue microarray. Expression of TBX5 in NSCLC tissues and cell lines was evaluated by quantitative PCR and Western blot. The role of TBX5 in regulating proliferation, colony formation,… More >

  • Open Access

    ARTICLE

    Examining the In Vitro Efficacy of the IAP Antagonist Birinapant as a Single Agent or in Combination With Dacarbazine to Induce Melanoma Cell Death

    Vesna Vetma*†‡, Jan Rožanc§, Emilie M. Charles*†, Christian T. Hellwig*†‡¶, Leonidas G. Alexopoulos§#, Markus Rehm*†‡#

    Oncology Research, Vol.25, No.9, pp. 1489-1494, 2017, DOI:10.3727/096504017X14897145996933

    Abstract Antagonists of inhibitors of apoptosis proteins (IAPs), alone or in combination with genotoxic therapeutics, have been shown to efficiently induce cell death in various solid tumors. The IAP antagonist birinapant is currently being tested in phase II clinical trials. We herein aimed to investigate the antitumor efficacy of dacarbazine in vitro, both as a single agent and in combination with birinapant, in melanoma cell lines. Covering clinically relevant drug concentration ranges, we conducted a total of 5,400 measurements in a panel of 12 human melanoma cell lines representing different stages of disease progression. Surprisingly, functionally More >

  • Open Access

    ARTICLE

    Cyclin-Dependent Kinase Inhibitor 3 Promotes Cancer Cell Proliferation and Tumorigenesis in Nasopharyngeal Carcinoma by Targeting p27

    Huimin Wang*, Hexin Chen, Hang Zhou*, Wenfa Yu*, Zhenmin Lu*

    Oncology Research, Vol.25, No.9, pp. 1431-1440, 2017, DOI:10.3727/096504017X14835311718295

    Abstract Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that arises from the nasopharynx epithelium and is highly invasive. Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dualspecificity protein phosphatase family, which plays a key role in regulating cell division. Abnormal expression of CDKN3 has been found in numerous types of cancer. In the current study, we explored the possible role of CDKN3 in cell proliferation, ability to invade, and radiosensitivity in NPC cells. We reported that CDKN3 was upregulated and p27 was downregulated in NPC tissues and is associated with a… More >

  • Open Access

    ARTICLE

    Gastrin Enhances Autophagy and Promotes Gastric Carcinoma Proliferation via Inducing AMPKα

    Zhuang Kun*†, Guo Hanqing*, Tang Hailing*, Yan Yuan*, Zhang Jun, Zhang Lingxia*, Han Kun*, Zhang Xin*

    Oncology Research, Vol.25, No.8, pp. 1399-1407, 2017, DOI:10.3727/096504016X14823648620870

    Abstract Gastric cancer (GC) is one of the most frequent epithelial malignancies worldwide. The gastrointestinal (GI) peptide gastrin is an important regulator of the secretion and release of gastric acid from stomach parietal cells, and it also plays a vital role in the development and progression of GC. The aim of the current study was to investigate the role and underlying mechanism of gastrin and autophagy in regulating GC tumorigenesis. Gastrin-17 amide (G-17) was applied in the GC cell lines SGC7901 and MGC-803. The results showed that G-17 maintained the high viability of SGC7901 and MGC-803.… More >

  • Open Access

    ARTICLE

    miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells

    Xiaoyu Wu*1, Jin Zhou†1, Zhenfeng Wu*, Che Chen*, Jiayun Liu*, Guannan Wu*, Jing Zhai*, Fukun Liu*, Gang Li

    Oncology Research, Vol.25, No.8, pp. 1383-1390, 2017, DOI:10.3727/096504017X14879366402279

    Abstract miR-101-3p has been identified as a tumor suppressor in several cancers, but its exact role in gastric adenocarcinoma is still largely unknown. In this study, we found that, compared with the RGM-1 human normal gastric epithelial cells, miR-101-3p was significantly downregulated in all six human gastric adenocarcinoma cell lines, including BGC-823, MNK-45, MGC-803, SGC-7901, AGS, and HGC-27. Overexpression of miR- 101-3p suppressed both the proliferation and invasion of AGS gastric adenocarcinoma cells, and knockdown of miR-101-3p displayed the opposite effect. In addition, miR-101-3p could directly target and suppress the expression of the serum response factor More >

  • Open Access

    ARTICLE

    Highly Expressed Antisense Noncoding RNA in the INK4 Locus Promotes Growth and Invasion of Renal Clear Carcinoma Cells via the β-Catenin Pathway

    Qingchun Li*, Yuan Tian, Guangrui Hu, Yun Liang, Wei Bai, Hongjun Li

    Oncology Research, Vol.25, No.8, pp. 1373-1382, 2017, DOI:10.3727/096504017X14878509668646

    Abstract Long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) is involved in several human cancers. However, the role of ANRIL in renal cell carcinoma (RCC) remains unclear. This study aimed to explore whether, and how, ANRIL affects the progression of RCC. First, the expression of ANRIL in clinical tumor tissues and four kinds of RCC cell lines was evaluated. After transfection, cell viability, colony number, apoptosis, migration, and invasion were assessed. The expression of proteins related to apoptosis, epithelial-tomesenchymal transition (EMT), and the β-catenin signaling pathway was then assessed. In addition, the… More >

  • Open Access

    ARTICLE

    Phase II Trial of Intensity-Modulated Radiotherapy Concurrent With Chemotherapy for Postoperative Node-Positive Esophageal Squamous Cell Carcinoma

    Hua Tao, Yiqin Zhou, Chengyun Yao, Dayong Gu, Wei Chen, Jincheng Lu

    Oncology Research, Vol.25, No.8, pp. 1357-1362, 2017, DOI:10.3727/096504017X14889842609577

    Abstract The aim of this study was to evaluate the efficacy and toxicity of intensity-modulated radiotherapy concurrent with weekly docetaxel in patients with node-positive esophageal squamous cell carcinoma after radical surgery. Between January 2011 and December 2013, a total of 46 eligible patients were enrolled. All patients received intensity-modulated radiotherapy concurrent with weekly docetaxel (20 mg/m2 ). Patients were treated 5 days per week at 2.0 Gy/day. The total dose of external radiotherapy given was 50 Gy in 25 fractions. The primary endpoints included treatment completion and safety. The secondary endpoint was to assess whether the approach… More >

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