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  • Open Access

    ARTICLE

    MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma

    Fang Chen*, Dongqiang Yang, Yuhua Ru, Shan Cao*, Aishe Gao*

    Oncology Research, Vol.27, No.6, pp. 691-701, 2019, DOI:10.3727/096504018X15426763753594

    Abstract Escalating evidence suggests that microRNA-101 (miR-101) is implicated in the development and progression of various cancers, including papillary thyroid carcinoma (PTC). However, the biological function and molecular mechanisms of miR-101 in PTC are still unclear. In this study, we demonstrated that miR-101 expression was significantly decreased in PTC tissues and cell lines. Clinically, a low level of miR-101 was positively associated with advanced histological stages and lymph node and distant metastases. The expression of CXCL12 was negatively correlated with miR-101 level in PTC. CXCL12 was validated as a direct target of miR-101 in PTC cells. More >

  • Open Access

    ARTICLE

    Long Noncoding RNA CAT104 Promotes Cell Viability, Migration, and Invasion in Gastric Carcinoma Cells Through Activation of MicroRNA-381-Inhibiting Zinc Finger E-box-Binding Homeobox 1 (ZEB1) Expression

    Gang Yuan, Jingzi Quan, Dongfang Dong, Qunying Wang

    Oncology Research, Vol.26, No.7, pp. 1037-1046, 2018, DOI:10.3727/096504017X15144748428127

    Abstract Gastric carcinoma (GC) remains the second leading cause of cancer-related deaths worldwide. Good biomarkers are of paramount importance for GC therapy. This study aimed to assess the role of long noncoding RNA (lncRNA) CAT104 in GC. We found that CAT104 was highly expressed in human GC NCI-N87, SGC7901, BGC823, BGC803, and AGS cells. Suppression of CAT104 decreased NCI-N87 cell viability, migration, and invasion, but promoted apoptosis. CAT104 knockdown enhanced the expression of microRNA- 381 (miR-381) expression in NCI-N87 cells. miR-381 participated in the regulatory effects of CAT104 on NCI-N87 cell viability, migration, invasion, and apoptosis. More >

  • Open Access

    ARTICLE

    MicroRNA-374a Promotes Hepatocellular Carcinoma Cell Proliferation by Targeting Mitogen-Inducible Gene 6 (MIG-6)

    Hui Li*1, Huicheng Chen†1, Haibin Wang, Yilong Dong, Min Yin, Liang Zhang§, Jia Wei*

    Oncology Research, Vol.26, No.4, pp. 557-563, 2018, DOI:10.3727/096504017X15000784459799

    Abstract Hepatocellular carcinoma (HCC) is a disease with poor prognosis rates and ineffective therapeutic options. Previous studies have reported the involvement of mitogen-inducible gene 6 (MIG-6) as a negative regulator in tumor formation. MicroRNAs (miRNAs) play crucial roles in the development of different types of cancer. However, the underlying mechanisms of miRNAs in HCC are poorly understood. This study was aimed to investigate the role of miR-374a in HCC and its role in the regulation of expression of MIG-6. The results showed that MIG-6 overexpression significantly inhibited cell viability of HepG2 cells after 4 days posttransfection. More >

  • Open Access

    ARTICLE

    Dexmedetomidine Inhibits Osteosarcoma Cell Proliferation and Migration, and Promotes Apoptosis by Regulating miR-520a-3p

    Xiaoyan Wang*, Yongguang Xu*, Xinlei Chen*, Jianmin Xiao

    Oncology Research, Vol.26, No.3, pp. 495-502, 2018, DOI:10.3727/096504017X14982578608217

    Abstract This study aimed to investigate the effect of dexmedetomidine (DEX) on osteosarcoma (OS) cell line MG63 and to explore the possible relationship between DEX and miR-520-3p in OS. The results showed that DEX could upregulate miR-520-3p, which directly targeted AKT1. Additionally, miR-520-3p also inhibited MG63 cell proliferation and migration, promoted apoptosis, and suppressed protein expressions of AKT, p-AKT, p-mTOR, and p-ERK1/2. DEX can inhibit OS cell proliferation and migration and promote apoptosis by upregulating the expression level of miR-520a-3p. DEX may serve as a potential therapeutic agent in OS treatment, and miR-520a-3p may be a More >

  • Open Access

    CORRECTION

    The Inhibitory Effects of HYDAMTIQ, a Novel PARP Inhibitor, on Growth in Human Tumor Cell Lines With Defective DNA Damage Response Pathways

    Enrico Mini*, Ida Landini*, Laura Lucarini, Andrea Lapucci*, Cristina Napoli, Gabriele Perrone*, Renato Tassi*, Emanuela Masini, Flavio Moroni, Stefania Nobili

    Oncology Research, Vol.26, No.2, pp. 333-334, 2018, DOI:10.3727/096504018X15187172557369

    Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

  • Open Access

    ARTICLE

    Procaine Inhibits the Proliferation and Migration of Colon Cancer Cells Through Inactivation of the ERK/MAPK/FAK Pathways by Regulation of RhoA

    Chang Li*, Shuohui Gao*, Xiaoping Li, Chang Li, Lianjun Ma§

    Oncology Research, Vol.26, No.2, pp. 209-217, 2018, DOI:10.3727/096504017X14944585873622

    Abstract Colon cancer is one of the most lethal varieties of cancer. Chemotherapy remains as one of the principal treatment approaches for colon cancer. The anticancer activity of procaine (PCA), which is a local anesthetic drug, has been explored in different studies. In our study, we aimed to explore the anticancer effect of PCA on colon cancer and its underlying mechanism. The results showed that PCA significantly inhibited cell viability, increased the percentage of apoptotic cells, and decreased the expression level of RhoA in HCT116 cells in a dose-dependent manner (p<0.05 or p<0.01). Moreover, PCA increased the… More >

  • Open Access

    ARTICLE

    The Inhibitory Effects of HYDAMTIQ, a Novel PARP Inhibitor, on Growth in Human Tumor Cell Lines With Defective DNA Damage Response Pathways

    Enrico Mini*, Ida Landini*, Laura Lucarini, Andrea Lapucci*, Cristina Napoli, Gabriele Perrone*, Renato Tassi*, Emanuela Masini, Flavio Moroni, Stefania Nobili

    Oncology Research, Vol.25, No.9, pp. 1441-1451, 2017, DOI:10.3727/096504017X14926854178616

    Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

  • Open Access

    ARTICLE

    Gamma Irradiation Upregulates B-cell Translocation Gene 2 to Attenuate Cell Proliferation of Lung Cancer Cells Through the JNK and NF-κB Pathways

    Peihe Wang*, Yuanyuan Cai*, Dongju Lin, Yingxiao Jiang*

    Oncology Research, Vol.25, No.7, pp. 1199-1205, 2017, DOI:10.3727/096504017X14873444858101

    Abstract Gamma ray can promote cancer cell apoptosis and cell cycle arrest. It is often used in the clinical treatment of tumors, including lung cancer. In this study, we aimed to explore the role of gamma ray treatment and its correlation with BTG2 in cell proliferation, apoptosis, and cell cycle arrest regulation in a lung cancer cell line. A549 cell viability, apoptosis rate, and cell cycle were investigated after gamma ray treatment. We then used siRNA for BTG2 to detect the effect of BTG2 knockdown on the progress of gamma ray-treated lung cancer cells. Finally, we… More >

  • Open Access

    ARTICLE

    Apigenin inhibits cell migration through MAPK pathways in human bladder smooth muscle cells

    QINGXIN LIU , XIANGGUI CHEN, GUOLIN YANG1 , XUEWEN MIN3 , AND MAOXIAN DENG1,*

    BIOCELL, Vol.35, No.3, pp. 71-80, 2011, DOI:10.32604/biocell.2011.35.071

    Abstract Apigenin, a nonmutagenic flavonoid, has been shown to possess free radical scavenging activities, anticarcinogenic properties, antioxidant and anti-inflammatory effects. Recently, apigenin was reported to cause gastric relaxation in murine. To assess possible effects of apigenin on migration of bladder smooth muscle (SM) cell, we isolated SM cells from peri-cancer tissue of human bladder and established a cell model that was capable to overexpress transiently MEKK1 (MEK kinase 1). Results showed that overexpression of active human MEKK1 by adenoviruses infection induced migration of human bladder smooth muscle (hBSM) cells and phosphorylation of MAPKs, ERK, JNK and More >

  • Open Access

    ARTICLE

    Apparent cross-talk of two signaling pathways that regulate Zea mays coleoptile growth

    Buentello Volante1 B, F Díaz de León-Sánchez1, F Rivera-Cabrera1, R Aguilar Caballero2, M Ponce-Valadez1, E Sánchez de Jiménez2, LJ Pérez-F lores1

    Phyton-International Journal of Experimental Botany, Vol.79, pp. 101-108, 2010, DOI:10.32604/phyton.2010.79.101

    Abstract Auxin and insulin promote Zea mays embryo growth, induce S6 ribosomal protein (S6rp) phosphorylation, and promote specific protein synthesis. The objective of this research was to test a possible cross-talk between insulin and auxin transduction pathways in Z. mays coleoptiles, typical auxin target tissues. Auxin and insulin produced differential quantitative and qualitative stimulation of cytoplasmic and ribosomal protein phosphorylation, and specific patterns of de novo synthesized cytoplasmic proteins. In addition, insulin induced S6rp phosphorylation was strongly inhibited by rapamycin, indicating target of rapamycin (TOR) kinase participation; auxin-induced S6rp phosphorylation was insensitive to this inhibitor. Phosphatidic acid (PA), a More >

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