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  • 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

    Protease Serine S1 Family Member 8 (PRSS8) Inhibits Tumor Growth In Vitro and In Vivo in Human Non-Small Cell Lung Cancer

    Chaonan Ma*1, Wei Ma*1, Nannan Zhou*, Na Chen*, Li An, Yijie Zhang*

    Oncology Research, Vol.25, No.5, pp. 781-787, 2017, DOI:10.3727/096504016X14772417575982

    Abstract Protease serine S1 family member 8 (PRSS8), a membrane-anchored serine protease, has been reported to be involved in the development of several human cancers. However, the role of PRSS8 in non-small cell lung cancer (NSCLC) pathogenesis remains unclear. The objective of this study was to investigate PRSS8 expression, biological function, and its related molecular mechanism in NSCLC. Our results showed that PRSS8 was expressed in a low amount in NSCLC cell lines. Ectopic expression of PRSS8 inhibited tumor growth in vitro and in vivo. Furthermore, ectopic expression of PRSS8 inhibited the migration and invasion of More >

  • Open Access

    ARTICLE

    Reduced Expression of Jumonji AT-Rich Interactive Domain 2 (JARID2) in Glioma Inhibits Tumor Growth In Vitro and In Vivo

    Zhenjiang Li*1, Chenyang Xu*1, Ming Gao*, Bingqian Ding*, Xinting Wei, Nan Ji

    Oncology Research, Vol.25, No.3, pp. 365-372, 2017, DOI:10.3727/096504016X14738135889976

    Abstract Jumonji AT-rich interactive domain 2 (JARID2) is a member of the Jumonji family of proteins and has been proposed as an oncogene in several types of human cancer. However, the role of JARID2 in human glioma has not yet been understood. The present study was designed to determine the roles of JARID2 in the proliferation and migration in human glioma cells and the growth of glioma cells in nude mice. Our data indicate that JARID2 is upregulated in human glioma tissues and cell lines. Knockdown of JARID2 obviously inhibits the proliferation of U87MG cells and More >

  • Open Access

    ARTICLE

    MicroRNA-139-3p Suppresses Tumor Growth and Metastasis in Hepatocellular Carcinoma by Repressing ANXA2R

    Zeng Cheng Zou*1, Min Dai*1, Zeng Yin Huang, Yi Lu, He Ping Xie*, Yi Fang Li§, Yue Li*, Ying Tan, Feng Lin Wang*

    Oncology Research, Vol.26, No.9, pp. 1391-1399, 2018, DOI:10.3727/096504018X15178798885361

    Abstract The direct roles of miR-139-3p on hepatocellular carcinoma (HCC) cell growth and metastasis remain poorly understood. We attempted to demonstrate the regulatory role of miR-139-3p in HCC progression and its underlying mechanisms. Here we showed that miR-139-3p expression was significantly reduced in the HCC tissues compared to paratumor tissues. Exogenous overexpression of miR-139-3p inhibited the migration and invasion of HCC cells, whereas downregulation of miR-139-3p was able to induce HCC HepG2 and SNU-449 cell migration and invasion. In addition, miR-139-3p inhibited HCC growth and lung metastasis in an in vivo mouse model, which is mainly More >

  • Open Access

    ARTICLE

    Downregulated Trophinin-Associated Protein Plays a Critical Role in Human Hepatocellular Carcinoma Through Upregulation of Tumor Cell Growth and Migration

    Yifan Lian*1, Weiming Fan†1, Yanlin Huang, Hongbo Wang*, Jialiang Wang*, Liang Zhou, Xiaojuan Wu, Meihai Deng, Yuehua Huang*‡

    Oncology Research, Vol.26, No.5, pp. 691-701, 2018, DOI:10.3727/096504017X15101398724809

    Abstract Trophinin-associated protein (TROAP) was a protein first identified to mediate the process of embryo transplantation and later found to be involved in microtubule regulation. However, little is known about the role of TROAP in hepatocellular carcinoma (HCC). In the present study, we reported that both TROAP mRNA and protein expressions were downregulated in human HCC samples as well as cell lines. A high level of TROAP was associated with small tumor size (p<0.05), minor tumor nodules (p<0.01), and mild vein invasion (p<0.05). We further constructed in vitro TROAP depletion and overexpression HCC cell models. TROAP depletion significantly More >

  • Open Access

    ARTICLE

    Proteasome Inhibitor MG132 Enhances Cisplatin-Induced Apoptosis in Osteosarcoma Cells and Inhibits Tumor Growth

    Farui Sun*, Yuanjin Zhang*, Lijun Xu*, Songbai Li*, Xiang Chen*, Ling Zhang*, Yifan Wu, Jun Li*

    Oncology Research, Vol.26, No.4, pp. 655-664, 2018, DOI:10.3727/096504017X15119525209765

    Abstract Although cisplatin has been shown to be an integral part of chemotherapy regimen in osteosarcoma (OS) treatment, toxicity issues and chemoresistance have hindered therapeutic development for OS. Exploring novel combination therapy methods is needed to circumvent the limitations of cisplatin alone. The proteasome inhibitor MG132 has shown antitumor effects in many solid tumors. However, little is known about its effects in combination with cisplatin in OS cells. In this study, we examined the effects of MG132 in combination with cisplatin in human OS cells (MG-63 and HOS). MG132 and cisplatin were applied to OS cells,… More >

  • Open Access

    ARTICLE

    G-Protein Signaling Protein-17 (RGS17) Is Upregulated and Promotes Tumor Growth and Migration in Human Colorectal Carcinoma

    Ling Li, He-Sheng Luo

    Oncology Research, Vol.26, No.1, pp. 27-35, 2018, DOI:10.3727/096504017X14900515946914

    Abstract Colorectal carcinoma is one of the leading causes of cancer-related deaths and has a high tendency for metastasis, which makes it a priority to find novel methods to diagnose and treat colorectal carcinoma at a very early stage. We studied the role of the regulator of G-protein signaling (RGS) family of proteins RGS17 in colorectal carcinoma growth and metastasis. We found that RGS17 was upregulated in both clinical colorectal carcinoma tissues and cultured colorectal carcinoma cells. Knockdown of RGS17 by specific siRNA decreased the cell proliferation rate, whereas overexpression of RGS17 with expression plasmid increased More >

  • Open Access

    ARTICLE

    Knockdown of HE4 suppresses tumor growth and invasiveness in lung adenocarcinoma through regulation of EGFR signaling

    YUE ZHANG1,#, WENYU YANG1,#, XIAOWANG HAN1,#, YUE QIAO1, HAITAO WANG2, TING CHEN1, TIANYING LI1, WEN-BIN OU1,*

    Oncology Research, Vol.32, No.6, pp. 1119-1128, 2024, DOI:10.32604/or.2024.045025

    Abstract It has been shown that the high expression of human epididymis protein 4 (HE4) in most lung cancers is related to the poor prognosis of patients, but the mechanism of pathological transformation of HE4 in lung cancer is still unclear. The current study is expected to clarify the function and mechanism of HE4 in the occurrence and metastasis of lung adenocarcinoma (LUAD). Immunoblotting evaluated HE4 expression in lung cancer cell lines and biopsies, and through analysis of The Cancer Genome Atlas (TCGA) dataset. Frequent HE4 overexpression was demonstrated in LUAD, but not in lung squamous… More >

  • Open Access

    ARTICLE

    GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling

    TINGTING LI1, WEI ZHONG1, LIU YANG1, ZHIYU ZHAO1, LI WANG1, CONG LIU1, WANYUN LI1, HAIYAN LV2, SHENGYU WANG1, JIANGHUA YAN1, TING WU1,*, GANG SONG1,*, FANGHONG LUO1,*

    Oncology Research, Vol.32, No.2, pp. 361-371, 2024, DOI:10.32604/or.2023.043807

    Abstract The high mortality rate associated with gastric cancer (GC) has resulted in an urgent need to identify novel therapeutic targets for GC. This study aimed to investigate whether GAIP interacting protein, C terminus 1 (GIPC1) represents a therapeutic target and its regulating mechanism in GC. GIPC1 expression was elevated in GC tissues, liver metastasis tissues, and lymph node metastases. GIPC1 knockdown or GIPC1 blocking peptide blocked the platelet-derived growth factor receptor (PDGFR)/PI3K/AKT signaling pathway, and inhibited the proliferation and migration of GC cells. Conversely, GIPC1 overexpression markedly activated the PDGFR/PI3K/AKT signaling pathway, and promoted GC More > Graphic Abstract

    GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling

  • Open Access

    ARTICLE

    UCHL5 inhibits U251 glioma cell proliferation and tumor growth via stabilizing and deubiquitinating PTEN

    YUE XIAO1,2,#, WENJING MA2,#, XINYI CHEN2, WEIWEI HU3, QIANQIAN DI2, XIBAO ZHAO2, GUODONG HUANG1, WEILIN CHEN1,2,*

    BIOCELL, Vol.47, No.12, pp. 2617-2625, 2023, DOI:10.32604/biocell.2023.042476

    Abstract Background: Glioma is the most common primary brain tumor. Exploration of new tumorigenesis mechanism of glioma is critical to determine more effective treatment targets as well as to develop effective prognosis methods that can enhance the treatment efficacy. We previously demonstrated that the deubiquitinase biquitin carboxyl-terminal hydrolase L5 (UCHL5) was downregulated in human glioma. However, the effect and mechanism of UCHL5 on the proliferation of glioma cells remains unknown. Methods: Transfection of siRNA was used to knockdown the expression of UCHL5 in U251 cells. The 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, Edu assay, and colony formation… More > Graphic Abstract

    UCHL5 inhibits U251 glioma cell proliferation and tumor growth via stabilizing and deubiquitinating PTEN

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