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Search Results (12)
  • 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 cell proliferation and migration. Furthermore,… 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 assay were employed to… More > Graphic Abstract

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

  • Open Access

    ARTICLE

    MicroRNA 615-3p Inhibits the Tumor Growth and Metastasis of NSCLC via Inhibiting IGF2

    Jiangtao Liu*, Yanli Jia*, Lijuan Jia*, Tingting Li, Lei Yang, Gongwen Zhang

    Oncology Research, Vol.27, No.2, pp. 269-279, 2019, DOI:10.3727/096504018X15215019227688

    Abstract MicroRNAs are essential regulators of cancer-associated genes at the posttranscriptional level, and their expression is altered in cancer tissues. Herein we sought to identify the regulation of miR-615-3p in NSCLC progression and its mechanism. miR-615-3p expression was significantly downregulated in NSCLC tissue compared to control normal tissue. Exogenous overexpression of miR-615-3p inhibited the growth and metastasis of NSCLC cells. In addition, the in vivo mouse xenograft model showed that overexpression of miR- 615-3p inhibited NSCLC growth and lung metastasis, whereas decreased expression of miR-615-3p caused an opposite outcome. Furthermore, we revealed that insulin-like growth factor 2 (IGF2) expression was negatively… More >

  • Open Access

    ARTICLE

    miR-223-5p Suppresses Tumor Growth and Metastasis in Non-Small Cell Lung Cancer by Targeting E2F8

    Liyan Dou*1, Kaiyu Han†1, Mochao Xiao*, Fuzhen Lv

    Oncology Research, Vol.27, No.2, pp. 261-268, 2019, DOI:10.3727/096504018X15219188894056

    Abstract miR-223-5p has been demonstrated to regulate the development and progression of various cancers, such as hepatocellular carcinoma, breast cancer, and gastric carcinoma. However, the role of miR-223-5p in nonsmall cell lung cancer (NSCLC) requires further investigation. In this study, we found that the expression of miR-223-5p was significantly downregulated in NSCLC tissues and cell lines. Moreover, the expression level of miR-223-5p is negatively correlated with the malignance of NSCLC. We found that overexpression of miR-223-5p remarkably suppressed the proliferation of NSCLC cells in vitro and in vivo. miR-223-5p overexpression also led to reduced migration and invasion in NSCLC cells. Mechanistically,… More >

  • Open Access

    ARTICLE

    miR-449a Suppresses Tumor Growth, Migration, and Invasion in Non-Small Cell Lung Cancer by Targeting a HMGB1-Mediated NF-kB Signaling Pathway

    Dandan Wu*1, Jun Liu†1, Jianliang Chen*, Haiyan He*, Hang Ma*, Xuedong Lv*

    Oncology Research, Vol.27, No.2, pp. 227-235, 2019, DOI:10.3727/096504018X15213089759999

    Abstract MicroRNAs (miRNAs) have been reported to be involved in many human cancers and tumor progression. The dysregulation of miR-449a is found in many types of malignancies and is associated with tumor growth, migration, and invasion. However, its expression and function in non-small cell lung cancer (NSCLC) still remains unclear. In our study, miR-449a was found to be downregulated in both NSCLC tissues and cell lines, and low miR-449a expression was obviously associated with tumor differentiation, TMN stage, and poor overall survival (OS). Moreover, we demonstrated that miR-449a could inhibit tumor proliferation, migration, and invasion in NSCLC. We also confirmed that… More >

  • Open Access

    ARTICLE

    miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

    Xiyan Sun*1, Chao Zhang†1, Yang Cao, Erbiao Liu*

    Oncology Research, Vol.27, No.3, pp. 317-323, 2019, DOI:10.3727/096504018X15228863026239

    Abstract miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there was an inverse correlation between… More >

  • Open Access

    ARTICLE

    EIF5A2 Is Highly Expressed in Anaplastic Thyroid Carcinoma and Is Associated With Tumor Growth by Modulating TGF-β Signals

    Fengyun Hao*1, Qingli Zhu, Lingwei Lu, Shukai Sun, Yichuan Huang§, Jinna Zhang, Zhaohui Liu†#, Yuanqing Miao**, Xuelong Jiao††, Dong Chen††1

    Oncology Research, Vol.28, No.4, pp. 345-355, 2020, DOI:10.3727/096504020X15834065061807

    Abstract Anaplastic thyroid carcinoma (ATC) is resistant to standard therapies and has no effective treatment. Eukaryotic translation initiation factor 5A2 (EIF5A2) has shown to be upregulated in many malignant tumors and proposed to be a critical gene involved in tumor metastasis. In this study, we aimed to investigate the expression status of EIF5A2 in human ATC tissues and to study the role and mechanisms of EIF5A2 in ATC tumorigenesis in vitro and in vivo. Expression of EIF5A2 protein was analyzed in paraffin-embedded human ATC tissues and adjacent nontumorous tissues (ANCT) (n = 24) by immunochemistry. Expressions of EIF5A2 mRNA and protein… More >

  • Open Access

    ARTICLE

    Tet methylcytosine dioxygenase 2 suppresses renal cell cancer proliferation and metastasis by regulating the miR-200c-SCD axis

    BENJIANG QIAN1, YOUFENG HUANG2, ZHENQIANG QIU2, XIAOYAN YING3, GUANG YANG3, HUIZHANG LI2,*, JIANMING TAN1,*

    BIOCELL, Vol.45, No.3, pp. 599-615, 2021, DOI:10.32604/biocell.2021.014633

    Abstract Tet methylcytosine dioxygenase 2 (TET2) acts as an antioncogene that is investigated in different cancers. But the effects of TET2 in renal cell cancer (RCC) is still known little. Here, quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescence were performed to exam gene and protein expression. Cell proliferation was measured using Cell Counting Kit-8 (CCK-8). Transwell assay was performed to detect cell metastasis viability. Flow cytometry was performed to analyze the cell cycle and cell apoptosis. The effects of TET2 on RCC growth in vivo was analyzed using a mouse xenograft model.We found that TET2 and miR-200c were decreased in… More >

  • Open Access

    ABSTRACT

    Experimental and Analytical Studies of Tumor Growth

    Hao Sun1, Timothy Eswothy1, Kerlin P. Robert1, Jiaoyan Li2, L. G. Zhang1, James D. Lee1,*

    Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 75-75, 2019, DOI:10.32604/mcb.2019.07090

    Abstract Most biological phenomena commonly involve with mechanics. In this work, we proposed an innovative model that tumor is considered as a pyroelastic medium consisting of two parts: solid and fluid. The variation of solid part depends on whether the drug has been effectively delivered to the tumor site. We derived the governing equations of the tumor, in which large deformation is incorporated. Meanwhile, the finite element equations for coupled displacement field and pressure field are formulated. We proposed two sets of porosity and growth tensor. In both cases the continuum theory and FEM are accompanied by accurate numerical simulations. To… More >

  • Open Access

    ARTICLE

    Role of Tumor Microvessel Architecture and Function in Chemotherapeutic Drug Delivery: A Three-Dimensional Numerical Study

    Yan Cai1,1, Zhiyong Li1,2,*

    Molecular & Cellular Biomechanics, Vol.14, No.2, pp. 59-81, 2017, DOI:10.3970/mcb.2017.014.057

    Abstract To investigate the dynamic changes of solid tumor and neo-vasculature in response to chemotherapeutic agent, we proposed a multi-discipline three-dimensional mathematical model by coupling tumor growth, angiogenesis, vessel remodelling, microcirculation and drug delivery. The tumor growth is described by the cell automaton model, in which three cell phenotypes (proliferating cell, quiescent cell and necrotic cell) are assumed to reflect the dynamics of tumor progress. A 3D tree-like architecture network with different orders for vessel diameter is generated as pre-existing vasculature in host tissue. The chemical substances including oxygen, vascular endothelial growth factor, extra-cellular matrix and matrix degradation enzymes are calculated… More >

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