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  • Open Access

    ARTICLE

    A Novel Fracturing Fluid with High-Temperature Resistance for Ultra-Deep Reservoirs

    Lian Liu1,2, Liang Li1,2, Kebo Jiao1,2,*, Junwei Fang1,2, Yun Luo1,2

    FDMP-Fluid Dynamics & Materials Processing, Vol.20, No.5, pp. 975-987, 2024, DOI:10.32604/fdmp.2023.030109

    Abstract Ultra-deep reservoirs play an important role at present in fossil energy exploitation. Due to the related high temperature, high pressure, and high formation fracture pressure, however, methods for oil well stimulation do not produce satisfactory results when conventional fracturing fluids with a low pumping rate are used. In response to the above problem, a fracturing fluid with a density of 1.2~1.4 g/cm was developed by using Potassium formatted, hydroxypropyl guanidine gum and zirconium crosslinking agents. The fracturing fluid was tested and its ability to maintain a viscosity of 100 mPa.s over more than 60 min More >

  • Open Access

    ARTICLE

    Astragaloside IV Enhances Cisplatin Chemosensitivity in Human Colorectal Cancer via Regulating NOTCH3

    Tao Xie*, Yao Li, Shi-Lei Li*, Hai-Feng Luo

    Oncology Research, Vol.24, No.6, pp. 447-453, 2016, DOI:10.3727/096504016X14685034103590

    Abstract Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined… More >

  • Open Access

    ARTICLE

    Anexelekto (AXL) Increases Resistance to EGFR-TKI and Activation of AKT and ERK1/2 in Non-Small Cell Lung Cancer Cells

    Yaqiong Tian*1, Zengli Zhang†1, Liyun Miao*, Zhimin Yang, Jie Yang*, Yinhua Wang§, Danwen Qian, Hourong Cai*, Yongsheng Wang*

    Oncology Research, Vol.24, No.5, pp. 295-303, 2016, DOI:10.3727/096504016X14648701447814

    Abstract Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and… More >

  • Open Access

    ARTICLE

    Knockdown of PARP-1 Inhibits Proliferation and ERK Signals, Increasing Drug Sensitivity in Osteosarcoma U2OS Cells

    Sheng Li, Zhengli Cui, Xianfeng Meng

    Oncology Research, Vol.24, No.4, pp. 279-286, 2016, DOI:10.3727/096504016X14666990347554

    Abstract Poly(ADP-ribose) polymerase 1 (PARP-1) is reported to be involved in DNA repair and is now recognized as a key regulator in carcinogenesis. However, the potential role and the molecular mechanism underlying the effect of PARP-1 on osteosarcoma (OS) cells have not been elucidated. In this study, the results showed that knockdown of PARP-1 resulted in decreased cell proliferation, increased cell apoptosis, and G0/G1 phase arrest in U2OS cells. In addition, increased expression of active caspase 3 and Bax, but reduced Bcl-2, cyclin D1, and phosphorylated extracellular signal regulated kinase 1/2 (pERK1/2) were observed in PARP-1 knockdown More >

  • Open Access

    ARTICLE

    Induction of Multidrug Resistance of Acute Myeloid Leukemia Cells by Cocultured Stromal Cells via Upregulation of the PI3K/Akt Signaling Pathway

    Ping Chen*, Qing Jin*, Qiang Fu*, Peidong You*, Xi Jiang*, Qin Yuan*, Huifang Huang

    Oncology Research, Vol.24, No.4, pp. 215-223, 2016, DOI:10.3727/096504016X14634208143021

    Abstract This study aimed to investigate the role of the PI3K/Akt signaling pathway in multidrug resistance of acute myeloid leukemia (AML) cells induced by cocultured stromal cells. Human AML cell lines HL-60 and U937 were adhesion cocultured with human bone marrow stromal cell line HS-5 cells. Such coculturing induced HL-60 and U937 cells resistant to chemotherapeutic drugs including daunorubicin (DNR), homoharringtonine (HHT), and cytosine arabinoside (Ara-C). The coculturing-induced resistance of AML cells to DNR, HHT, and Ara-C can be partially reversed by inhibition of the PI3K/Akt signaling pathway. Clinically, AML patients with a low level of More >

  • Open Access

    ARTICLE

    Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Lung Cancer Cells and Inhibits Regulating Epithelial-to-Mesenchymal Transition

    Shenggang Liu*, Hongzhong Yang, Ying Chen, Baimei He§, Qiong Chen§

    Oncology Research, Vol.24, No.2, pp. 81-87, 2016, DOI:10.3727/096504016X14597766487717

    Abstract In order to improve therapeutic efficacy, it is a current emergency to better know the mechanisms underlying cisplatin resistance in lung cancer cells. In this study, we aim to investigate the role of Krüppel-like factor 4 (KLF4) in cisplatin-resistant lung cancer cells. We developed cisplatin-resistant lung cancer cell line A549/ DDP, and then a battery of experiments was used to analyze the effects of KLF4 in cisplatin resistance of lung cancer. We found that KLF4 was significantly downregulated in cisplatin-resistant A549 cells and forced KLF4 expression inhibited cell growth and induced apoptosis. Further, we found More >

  • Open Access

    ARTICLE

    Inhibitors of PI3K/ERK1/2/p38 MAPK Show Preferential Activity Against Endocrine-Resistant Breast Cancer Cells

    Maitham A. Khajah, Princy M. Mathew, Yunus A. Luqmani

    Oncology Research, Vol.25, No.8, pp. 1283-1295, 2017, DOI:10.3727/096504017X14883245308282

    Abstract Current mainstream pharmacological options for the treatment of endocrine-resistant breast cancer have limitations in terms of their side effect profile and lack of discrimination between normal and cancer cells. In the current study, we assessed the responses of normal breast epithelial cells MCF10A, estrogen receptorpositive (ER+ ) MCF-7, and ER-silenced pII breast cancer cells to inhibitors (either individually or in combination) of downstream signaling molecules. The expression/activity of ERK1/2, p38 MAPK, and Akt was determined by Western blotting. Cell proliferation, motility, and invasion were determined using MTT, wound healing, and Matrigel assays, respectively. Morphological changes… More >

  • Open Access

    ARTICLE

    Histone Acetyltransferase 1 Promotes Cell Proliferation and Induces Cisplatin Resistance in Hepatocellular Carcinoma

    Xin Jin*, Shenghua Tian, Pingping Li

    Oncology Research, Vol.25, No.6, pp. 939-946, 2017, DOI:10.3727/096504016X14809827856524

    Abstract Hepatocellular carcinoma (HCC) is one of the most common malignant diseases in the world. Mutations, overexpression, and improper recruitment of HATs can lead to tumorigenesis. HAT1 is the first histone acetyltransferase identified and is related with developing HCC, but the mechanism is still unclear. Interestingly, we found that HAT1 was upregulated in HCC patient specimens and showed that its upregulation facilitates HCC cell growth in vitro and in vivo. Moreover, we demonstrated that HAT1 promoted glycolysis in HCC cells and knockdown of HAT1 sensitized HCC cells to apoptotic death induced by cisplatin. Our results suggest More >

  • Open Access

    ARTICLE

    CLIC1 Induces Drug Resistance in Human Choriocarcinoma Through Positive Regulation of MRP1

    Jinhui Wu, Dongshuang Wang

    Oncology Research, Vol.25, No.6, pp. 863-871, 2017, DOI:10.3727/096504016X14772315906527

    Abstract Chemotherapy is typically used to treat choriocarcinoma. However, a small proportion of this malignancy develops resistance to common chemotherapeutic drugs such as methotrexate (MTX) and floxuridine (FUDR). This study aimed to investigate the role and potential mechanisms of chloride intracellular channel protein 1 (CLIC1) in the development of chemoresistance in choriocarcinoma JeG3 cells. Two chemoresistant sublines were induced from their parental cell line JeG3 through intermittent exposure to MTX (named JeG3/MTX) or FUDR (named JeG3/FUDR). It was found that expression of CLIC1 was significantly higher in the chemoresistant sublines JeG3/MTX and JeG3/FUDR than in their… More >

  • Open Access

    ARTICLE

    Silencing of Btbd7 Inhibited Epithelial–Mesenchymal Transition and Chemoresistance in CD133+ Lung Carcinoma A549 Cells

    Li-Zhou Fang*, Jian-Qing Zhang*, Ling Liu*, Wei-Ping Fu*, Jing-Kui Shu*, Jia-Gang Feng*, Xiao Liang

    Oncology Research, Vol.25, No.5, pp. 819-829, 2017, DOI:10.3727/096504016X14772349843854

    Abstract Cancer stem cells (CSCs) are responsible for tumorigenesis and recurrence, so targeting CSCs is an effective method to potentially cure cancer. BTB/POZ domain-containing protein 7 (Btbd7) has been found in various cancers, including lung cancer and liver cancer, but the role of Btbd7 in non-small cell lung cancer (NSCLC), CSC self-renewal, and chemoresistance is still unknown. Therefore, in this study we found that the ratio of tumor sphere formation and stem cell transcription factors in CD133+ cells was dramatically enhanced compared to parental cells, which indicated successful sorting of CD133+ cells from A549. Meanwhile, Btbd7 and More >

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