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  • Open Access

    ARTICLE

    NET1 Enhances Proliferation and Chemoresistance in Acute Lymphoblastic Leukemia Cells

    Hongbo Sun*1, Zhifu Zhang*1, Wei Luo*, Junmin Liu*, Ye Lou, Shengmei Xia

    Oncology Research, Vol.27, No.8, pp. 935-944, 2019, DOI:10.3727/096504019X15555388198071

    Abstract Acute lymphoblastic leukemia (ALL) is the most prevalent of pediatric cancers. Neuroepithelial cell-transforming 1 (NET1) has been associated with malignancy in a number of cancers, but the role of NET1 in ALL development is unclear. In the present study, we investigated the effect of NET1 gene in ALL cell proliferation and chemoresistance. We analyzed GEO microarray data comparing bone marrow expression profiles of pediatric B-cell ALL samples and those of age-matched controls. MTT and colony formation assays were performed to analyze cell proliferation. ELISA assays, Western blot analyses, and TUNEL staining were used to detect chemoresistance. We confirmed that NET1… More >

  • Open Access

    ARTICLE

    PPARb/d Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by Regulating miR-206

    Linglan Gu, Yi Shi, Weimin Xu, Yangyang Ji

    Oncology Research, Vol.27, No.8, pp. 923-933, 2019, DOI:10.3727/096504019X15518706875814

    Abstract In previous investigations, we reported that peroxisome proliferator-activated receptor / (PPAR / ) activation by GW501516 inhibits proliferation and promotes apoptosis in the undifferentiated C666-1 nasopharyngeal carcinoma (NPC) cells by modulating caspase-dependent apoptotic pathway. In the present study, the mechanism by which GW501516 induces apoptosis was explored from the perspective of microRNA (miRNA) expression. Among the assayed miRNAs that were involved in regulating the expression of antiapoptotic protein Bcl-2, miR-206 was increased significantly and specifically by GW501516 in C666-1 cells at both the in vitro level and at the in vivo xenograft samples. The induction on miR-206 expression caused by… More >

  • Open Access

    ARTICLE

    miR-148-3p Inhibits Growth of Glioblastoma Targeting DNA Methyltransferase-1 (DNMT1)

    Yongtao Li*, Fanyu Chen*, Jiancheng Chu*, Chao Wu*, Yuan Li, Heng Li, Hongxin Ma*

    Oncology Research, Vol.27, No.8, pp. 911-921, 2019, DOI:10.3727/096504019X15516966905337

    Abstract To date, miR-148-3p and DNMT1–recombinant human runt-related transcription factor 3 (RUNX3) axis have been linked to cell proliferation, migration, and invasion; however, their roles and relationships in human glioblastoma multiforme (GBM) are still not clear. Here we found that the expression of miR-148-3p in glioma tissues was decreased compared with adjacent nontumor tissues and correlated with WHO grade, tumor size, and prognosis as well as DNMT1 and RUNX3 expressions. Compared with NHA cells, the expression of miR- 148-3p in U87 and U251 cells was also downregulated and accompanied with upregulation of DNMT1 and hypermethylation level of RUNX3 promoter region. miR-148-3p… More >

  • Open Access

    ARTICLE

    Different Types of ROS1 Fusion Partners Yield Comparable Efficacy to Crizotinib

    Yueming He*1, Wang Sheng†1, Weiguo Hu‡1, Jing Lin§, Junjun Liu§, Bing Yu§, Xinru Mao§, Lu Zhang§, Jin Huang, Guangsuo Wang#

    Oncology Research, Vol.27, No.8, pp. 901-910, 2019, DOI:10.3727/096504019X15509372008132

    Abstract ROS1 rearrangements define a distinct molecular subset of non-small-cell lung cancer (NSCLC), which can be treated effectively with crizotinib, a tyrosine kinase inhibitor (TKI) targeting ROS1/MET/ALK rearrangements. Diverse efficacy was observed in ROS1-rearranged NSCLC patients. Because of its rareness, very limited studies have investigated the correlation between different fusion partners and response to crizotinib. In this study, we retrospectively screened 6,235 advanced NSCLC patients (stage IIIB to IV) from five hospitals and identified 106 patients with ROS1 rearrangements based on either plasma or tumor tissue testing using capturebased targeted sequencing. The most frequently occurring fusion partners included cluster of differentiation… More >

  • Open Access

    ARTICLE

    Anticancer Effects of Gleditsia sinensis Extract in Rats Transplanted With Hepatocellular Carcinoma Cells

    Yue Cai*†‡, Chizhi Zhang*†‡, Lei Zhan*†, Liangbin Cheng*†, Dingbo Lu*†, Xiaodong Wang*†, Hanlin Xu§, Shuxue Wang, Deng Wu*†, Lianguo Ruan#

    Oncology Research, Vol.27, No.8, pp. 889-899, 2019, DOI:10.3727/096504018X15482423944678

    Abstract The thorns of Gleditsia sinensis have been historically used in Chinese medicine and are considered one of the fundamental therapeutic herbs. Its anticancer effects are currently being explored. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and still requires the development of new drugs with higher efficiency. By using a rat HCC model implanted with cancerous Walker-256 cells, the therapeutic effects of G. sinensis extract (GSE) were assessed, as well as its regulatory effects on miRNAs. GSE significantly restored liver morphology and dramatically induced cell apoptosis in HCC rats. In addition, miR-21/181b/183 was upregulated in the… More >

  • Open Access

    ARTICLE

    MicroRNA-510 Plays Oncogenic Roles in Non-Small Cell Lung Cancer by Directly Targeting SRC Kinase Signaling Inhibitor 1

    Wei Wu*, Linyan He†‡, Yan Huang*, Likun Hou*, Wei Zhang*, Liping Zhang*, Chunyan Wu*

    Oncology Research, Vol.27, No.8, pp. 879-887, 2019, DOI:10.3727/096504018X15451308507747

    Abstract An increasing number of studies have demonstrated that microRNAs (miRNAs) may play key roles in various cancer carcinogenesis and progression, including non-small cell lung cancer (NSCLC). However, the expressions, roles, and mechanisms of miR-510 in NSCLC have, up to now, been largely undefined. In vivo assay showed that miR-510 was upregulated in NSCLC tissues compared with that in adjacent nontumor lung tissues. miR-510 expression was significantly correlated with TNM stage and lymph node metastasis. In vitro assay indicated that expressions of miR-510 were also increased in NSCLC cell lines. Downregulation of miR-510 suppressed NSCLC cell proliferation and invasion in vitro.… More >

  • Open Access

    ARTICLE

    Secreted Phosphoprotein 1 (SPP1) Contributes to Second-Generation EGFR Tyrosine Kinase Inhibitor Resistance in Non-Small Cell Lung Cancer

    Xinwen Wang, Fupeng Zhang, Xi Yang, Meiping Xue, Xiaoli Li, Yu Gao, Likun Liu

    Oncology Research, Vol.27, No.8, pp. 871-877, 2019, DOI:10.3727/096504018X15426271404407

    Abstract Second-generation irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), afatinib, has been approved for treating EGFR mutant lung cancer patients, but the mechanism of acquired resistance to afatinib has not been well studied. In this study, we established afatinib acquired resistant cell lines. Gene array technology was used to screen changes in gene expression between afatinib-resistant lung cancer cells and parental cells. Our results showed that secreted phosphoprotein 1 (SPP1) was significantly increased in afatinib-resistant lung cancer cells. To study the effect of SPP1 on afatinib resistance, siSPP1 was used to knock down SSP1 in afatinib-resistant lung cancer… More >

  • Open Access

    ARTICLE

    Mitotic Arrest-Deficient Protein 2B Overexpressed in Lung Cancer Promotes Proliferation, EMT, and Metastasis

    Hua Zhang*, Xiuquan He, Wenfei Yu, Bingqing Yue, Ziting Yu, Ying Qin*

    Oncology Research, Vol.27, No.8, pp. 859-869, 2019, DOI:10.3727/096504017X15049209129277

    Abstract As the noncatalytic subunit of mammalian DNA polymerase, mitotic arrest-deficient protein 2B (MAD2B) has been reported to play a role in cell cycle regulation, DNA damage tolerance, gene expression, and carcinogenesis. Although its expression is known to be associated with poor prognosis in several types of human cancers, the significance of MAD2B expression in lung malignancies is still unclear. Our study showed that MAD2B expression significantly increased in lung cancer, especially in the metastatic tissues. We also found that knockdown of MAD2B inhibited the migration, invasion, and epithelial–mesenchymal transition of lung cancer cells in vitro and the metastasis in vivo,… More >

  • Open Access

    REVIEW

    The Roles of Plant-Derived Triptolide on Non-Small Cell Lung Cancer

    Jie Wei*†1, Yuanliang Yan*†1, Xi Chen*†, Long Qian*†, Shuangshuang Zeng*†, Zhi Li, Shuang Dai*†, Zhicheng Gong*†,Zhijie Xu§

    Oncology Research, Vol.27, No.7, pp. 849-858, 2019, DOI:10.3727/096504018X15447833065047

    Abstract Over the past decade, natural compounds have been proven to be effective against many human diseases, including cancers. Triptolide (TPL), a diterpenoid triepoxide from the Chinese herb Tripterygium wilfordii Hook F, has exhibited attractive cytotoxic activity on several cancer cells. An increasing number of studies have emphasized the antitumor effects of TPL on non-small cell lung cancer (NSCLC). Here we mainly focused on the key molecular signaling pathways that lead to the inhibitory effects of TPL on human NSCLC, such as mitogen-activated protein kinases (MAPKs) modulation, inhibition of NF- B activation, suppression of miRNA expression, etc. In addition, the effect… More >

  • Open Access

    ARTICLE

    Nonsteroidal Anti-inflammatory Drugs Sensitize CD44-Overexpressing Cancer Cells to Hsp90 Inhibitor Through Autophagy Activation

    Hyun-Jung Moon,1 So-Young Park,1 Su-Hoon Lee, Chi-Dug Kang, Sun-Hee Kim

    Oncology Research, Vol.27, No.7, pp. 835-847, 2019, DOI:10.3727/096504019X15517850319579

    Abstract Recently, novel therapeutic strategies have been designed with the aim of killing cancer stem-like cells (CSCs), and considerable interest has been generated in the development of specific therapies that target stemnessrelated marker of CSCs. In this study, nonsteroidal anti-inflammatory drugs (NSAIDs) significantly potentiated Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG)-mediated cytotoxicity through apoptotic and autophagic cell death induction, but COX-2-inhibitory function was not required for NSAIDinduced autophagy in CD44-overexpressing human chronic myeloid leukemia K562 (CD44highK562) cells. Importantly, we found that treatment with NSAIDs resulted in a dose-dependent increase in LC3-II level and decrease in p62 level and simultaneous reduction in multiple stemness-related markers… More >

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