Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (32)
  • 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

    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

    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

    miR-135a Confers Resistance to Gefitinib in Non-Small Cell Lung Cancer Cells by Upregulation of RAC1

    Tingting Zhang*1, Ning Wang†1

    Oncology Research, Vol.26, No.8, pp. 1191-1200, 2018, DOI:10.3727/096504018X15166204902353

    Abstract The EGFR tyrosine kinase inhibitor gefitinib is used in therapy for non-small cell lung cancer (NSCLC). However, the therapeutic efficacy of gefitinib is known to be impeded by mutations of EGFR. The aim of the present study was to reveal the role of miR-135a in gefitinib resistance of NSCLC cells. Human NSCLC cell lines, NCI-H1650 and NCI-H1975, were transfected with miR-135a mimic/inhibitor or miR-135a inhibitor plus pEX-RAC1 (a RAC1-expressing vector). The effects of miR-135a and RAC1 expression on cell viability, apoptosis, migration, and invasion were then detected. The transfected cells were exposed to 0–20 µM… More >

  • Open Access

    ARTICLE

    Micro-RNA-21 Regulates Cancer-Associated Fibroblast-Mediated Drug Resistance in Pancreatic Cancer

    Lulin Zhang, Jun Yao, Wenyao Li, Ce Zhang

    Oncology Research, Vol.26, No.6, pp. 827-836, 2018, DOI:10.3727/096504017X14934840662335

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer deaths due to its highly aggressive biological nature and resistance to chemotherapy. Previous studies indicate that miR-21 is an important regulator in the activation of cancer-associated fibroblasts (CAFs). However, whether miR-21 in CAFs would regulate PDAC’s tumor microenvironment and lead to drug resistance remain unknown. In this study, we evaluated the relationship between CAF activation, miR-21 expression, and drug resistance using tumor samples from PDAC patients. We changed the miR-21 expression level in CAFs and tested its roles in regulating the function of… More >

  • Open Access

    ARTICLE

    Long Noncoding RNA (lncRNA) HOTAIR Affects Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer by Upregulating miR-613

    Caiyu Jiang, Yan Yang, Yang Yang, Lu Guo, Jiang Huang, Xingren Liu, Chi Wu, Jun Zou

    Oncology Research, Vol.26, No.5, pp. 725-734, 2018, DOI:10.3727/096504017X15119467381615

    Abstract Non-small cell lung cancer (NSCLC) is one of the most deadly cancers with poor prognosis. Recent findings suggested that the lncRNA HOTAIR played an important role in tumorigenesis and metastasis. In the present study, HOTAIR was highly expressed in NSCLC tumor tissues and cell lines (H1299, H23, H292, and A549). Downregulation of HOTAIR suppressed cell proliferation and invasion, while it promoted apoptosis of NSCLC cells. The targeting relationship between HOTAIR and miR-613 was first revealed by bioinformatics prediction. miR-613 was found to be lowly expressed in NSCLC tumor tissues and cell lines. Knockdown of HOTAIR… More >

  • Open Access

    ARTICLE

    PHLDA2 reshapes the immune microenvironment and induces drug resistance in hepatocellular carcinoma

    KUN FENG1,#, HAO PENG2,#, QINGPENG LV1, YEWEI ZHANG1,*

    Oncology Research, Vol.32, No.6, pp. 1063-1078, 2024, DOI:10.32604/or.2024.047078

    Abstract Hepatocellular carcinoma (HCC) is a malignancy known for its unfavorable prognosis. The dysregulation of the tumor microenvironment (TME) can affect the sensitivity to immunotherapy or chemotherapy, leading to treatment failure. The elucidation of PHLDA2’s involvement in HCC is imperative, and the clinical value of PHLDA2 is also underestimated. Here, bioinformatics analysis was performed in multiple cohorts to explore the phenotype and mechanism through which PHLDA2 may affect the progression of HCC. Then, the expression and function of PHLDA2 were examined via the qRT-PCR, Western Blot, and MTT assays. Our findings indicate a substantial upregulation of… More >

  • Open Access

    REVIEW

    Deciphering resistance mechanisms and novel strategies to overcome drug resistance in ovarian cancer: a comprehensive review

    EFFAT ALEMZADEH1, LEILA ALLAHQOLI2, AFROOZ MAZIDIMORADI3, ESMAT ALEMZADEH1,4, FAHIMEH GHASEMI4,5, HAMID SALEHINIYA6, IBRAHIM ALKATOUT7,*

    Oncology Research, Vol.32, No.5, pp. 831-847, 2024, DOI:10.32604/or.2024.031006

    Abstract Ovarian cancer is among the most lethal gynecological cancers, primarily due to the lack of specific symptoms leading to an advanced-stage diagnosis and resistance to chemotherapy. Drug resistance (DR) poses the most significant challenge in treating patients with existing drugs. The Food and Drug Administration (FDA) has recently approved three new therapeutic drugs, including two poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and niraparib) and one vascular endothelial growth factor (VEGF) inhibitor (bevacizumab) for maintenance therapy. However, resistance to these new drugs has emerged. Therefore, understanding the mechanisms of DR and exploring new approaches to overcome More >

  • Open Access

    ARTICLE

    Extensive prediction of drug response in mutation-subtype-specific LUAD with machine learning approach

    KEGANG JIA1,#, YAWEI WANG2,#, QI CAO3,*, YOUYU WANG1,*

    Oncology Research, Vol.32, No.2, pp. 409-419, 2024, DOI:10.32604/or.2023.042863

    Abstract Background: Lung cancer is the most prevalent cancer diagnosis and the leading cause of cancer death worldwide. Therapeutic failure in lung cancer (LUAD) is heavily influenced by drug resistance. This challenge stems from the diverse cell populations within the tumor, each having unique genetic, epigenetic, and phenotypic profiles. Such variations lead to varied therapeutic responses, thereby contributing to tumor relapse and disease progression. Methods: The Genomics of Drug Sensitivity in Cancer (GDSC) database was used in this investigation to obtain the mRNA expression dataset, genomic mutation profile, and drug sensitivity information of NSCLS. Machine Learning… More >

Displaying 1-10 on page 1 of 32. Per Page