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Search Results (21)
  • 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

    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

    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

    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

    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

    Inhibition of Carbonic Anhydrase IX by Ureidosulfonamide Inhibitor U104 Reduces Prostate Cancer Cell Growth, But Does Not Modulate Daunorubicin or Cisplatin Cytotoxicity

    Anne Riemann*, Antje Güttler, Verena Haupt*, Henri Wichmann, Sarah Reime*, Matthias Bache, Dirk Vordermark, Oliver Thews*

    Oncology Research, Vol.26, No.2, pp. 191-200, 2018, DOI:10.3727/096504017X14965111926391

    Abstract Carbonic anhydrase (CA) IX has emerged as a promising target for cancer therapy. It is highly upregulated in hypoxic regions and mediates pH regulation critical for tumor cell survival as well as extracellular acidification of the tumor microenvironment, which promotes tumor aggressiveness via various mechanisms, such as augmenting metastatic potential. Therefore, the aim of this study was to analyze the complex interdependency between CA IX and the tumor microenvironment in prostate tumor cells with regard to potential therapeutic implications. CA IX was upregulated by hypoxia as well as acidosis in prostate cancer cells. This induction… More >

  • Open Access

    ARTICLE

    miR-125b reverses cisplatin resistance by regulating autophagy via targeting RORA/BNIP3L axis in lung adenocarcinoma

    LEI LIU1, NA GUO1, XIANGLING LI2, QIAN XU2, RUILONG HE3, LIMIN CHENG4, CHUNYAN DANG3, XINYU BAI3, YIYING BAI3, XIN WANG3, QIANHUI CHEN3, LI ZHANG3,*

    Oncology Research, Vol.32, No.4, pp. 643-658, 2024, DOI:10.32604/or.2023.044491

    Abstract The platinum-based chemotherapy is one of the most frequently used treatment protocols for lung adenocarcinoma (LUAD), and chemoresistance, however, usually results in treatment failure and limits its application in the clinic. It has been shown that microRNAs (miRNAs) play a significant role in tumor chemoresistance. In this study, miR-125b was identified as a specific cisplatin (DDP)-resistant gene in LUAD, as indicated by the bioinformatics analysis and the real-time quantitative PCR assay. The decreased serum level of miR-125b in LUAD patients was correlated with the poor treatment response rate and short survival time. MiR-125b decreased the… More >

  • Open Access

    ARTICLE

    TGF-β-regulated different iron metabolism processes in the development and cisplatin resistance of ovarian cancer

    JIANFA WU1,2,#, QIANYI LIAO3,#, LI ZHANG1,2,#, SUQIN WU1,2,*, ZHOU LIU1,2,*

    Oncology Research, Vol.32, No.2, pp. 373-391, 2024, DOI:10.32604/or.2023.031404

    Abstract The impact of different iron metabolism processes (DIMP) on ovarian cancer remains unclear. In this study, we employed various gene chips and databases to investigate the role of DIMP in the initiation and development of ovarian cancer. cBioPortal was used to determine mutations in DIMP-associated genes in ovarian cancer. Kaplan-Meier plotter was used to examine the influence of DIMP on the prognosis of ovarian cancer. By analyzing 1669 serous ovarian cancer cases, we identified a range of mutations in iron metabolism genes, notably in those coding for the transferrin receptor (19%), melanotransferrin (19%), and ceruloplasmin… More >

  • Open Access

    ARTICLE

    Cisplatin-induced activation of TGF-β signaling contributes to drug resistance

    SAYAKA IMATSUJI1,#, YUKIKO UJIE1,#, HIROYUKI ODAKE1, MASAYA IMOTO1,2, SUSUMU ITOH3, ETSU TASHIRO1,3,*

    Oncology Research, Vol.32, No.1, pp. 139-150, 2024, DOI:10.32604/or.2023.030190

    Abstract Growing evidence suggests an association between epithelial-mesenchymal transition (EMT), a hallmark of tumor malignancy, and chemoresistance to a number of anti-cancer drugs. However, the mechanism of EMT induction in the process of acquiring anti-cancer drug resistance remains unclear. To address this issue, we obtained a number of cisplatin-resistant clones from LoVo cells and found that almost all of them lost cell-cell contacts. In these clones, the epithelial marker E-cadherin was downregulated, whereas the mesenchymal marker N-cadherin was upregulated. Moreover, the expression of EMT-related transcription factors, including Slug, was elevated. On the other hand, the upregulation More >

  • Open Access

    ARTICLE

    Deciphering key genes involved in cisplatin resistance in kidney renal clear cell carcinoma through a combined in silico and in vitro approach

    MUNEEBA MALIK1, MAMOONA MAQBOOL2, TOOBA NISAR3, TAZEEM AKHTER4, JAVED AHMED UJAN5,6, ALANOOD S. ALGARNI7, FAKHRIA A. AL JOUFI8, SULTAN SHAFI K. ALANAZI9, MOHAMMAD HADI ALMOTARED10, MOUNIR M. SALEM BEKHIT11, MUHAMMAD JAMIL12,*

    Oncology Research, Vol.31, No.6, pp. 899-916, 2023, DOI:10.32604/or.2023.030760

    Abstract The low survival rate of Kidney renal clear cell carcinoma (KIRC) patients is largely attributed to cisplatin resistance. Rather than focusing solely on individual proteins, exploring protein-protein interactions could offer greater insight into drug resistance. To this end, a series of in silico and in vitro experiments were conducted to identify hub genes in the intricate network of cisplatin resistance-related genes in KIRC chemotherapy. The genes involved in cisplatin resistance across KIRC were retrieved from the National Center for Biotechnology Information (NCBI) database using search terms as “Kidney renal clear cell carcinoma” and “Cisplatin resistance”. The genes… More >

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