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  • Open Access

    ARTICLE

    VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin in Non-Small Cell Lung Cancer via AKT Signaling

    Xiangbin Tan*1, Zefei Liao†1, Shuangyou Zou*, Liangyun Ma, Aimin Wang*

    Oncology Research, Vol.28, No.1, pp. 3-11, 2020, DOI:10.3727/096504019X15509383469698

    Abstract Vasohibin2 (VASH2), a proangiogenic factor, has been demonstrated to play an oncogenic role in some common human cancers. However, the detailed function of VASH2 in non-small cell lung cancer (NSCLC) has not previously been studied. In this study, we found that VASH2 was significantly upregulated in NSCLC tissues and cell lines, and its increased expression was associated with NSCLC progression and poor prognosis of patients. Knockdown of VASH2 markedly inhibited cell proliferation and P-glycoprotein expression in NSCLC cells. Overexpression of VASH2 enhanced cell proliferation, P-glycoprotein expression, as well as doxorubicin resistance in NSCLC cells. Moreover,… More >

  • Open Access

    ARTICLE

    MicroRNA-708 inhibits the proliferation and chemoresistance of pancreatic cancer cells

    Wensong LIU1, Yunjie LU1, Dong ZHANG1, Longqing SHI1, Guangchen ZU1, Haijiao YAN2,*, Donglin SUN1,*

    BIOCELL, Vol.44, No.1, pp. 73-80, 2020, DOI:10.32604/biocell.2020.08613 - 01 March 2020

    Abstract Pancreatic cancer is one of the most aggressive malignancies with poor prognosis and high mortality. Recent studies showed that microRNAs are dysregulated and involved in the initiation and progression of pancreatic cancer. In this study, we found that miR-708 was significantly downregulated in pancreatic cancer tissues and cell lines. Lentivirus-mediated overexpression of miR-708 could significantly inhibit the proliferation and invasion, while enhanced chemosensitivity to gemcitabine in both Panc-1 and SW1990 cells. Luciferase reporter assay showed that miR-708 bound the 3’-untranslated region of survivin and suppressed the expression of survivin in pancreatic cancer cells. In pancreatic More >

  • Open Access

    ARTICLE

    TIMP-3 Increases the Chemosensitivity of Laryngeal Carcinoma to Cisplatin via Facilitating Mitochondria-Dependent Apoptosis

    Xiaohui Shen, Xia Gao, Hui Li, Yajun Gu, Junguo Wang

    Oncology Research, Vol.27, No.1, pp. 73-80, 2019, DOI:10.3727/096504018X15201099883047

    Abstract Laryngeal carcinoma is a type of head and neck carcinoma with a high incidence and mortality. Chemotherapy treatments of human laryngeal carcinoma may fail due to the development of chemoresistance. Tissue inhibitor of metalloproteinase 3 (TIMP-3) has been shown to be implicated in a number of pathological processes typical for cancer. The present study aims to investigate the involvement of TIMP-3 in the chemoresistance of laryngeal carcinoma. We showed that TIMP-3 expression was significantly decreased in chemoresistant laryngeal carcinoma tissues compared with chemosensitivity tissues. Patients with low TIMP-3 expression exhibited poorer overall survival than those… More >

  • 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… More >

  • Open Access

    ARTICLE

    Hsa_circ_0003998 Promotes Chemoresistance via Modulation of miR-326 in Lung Adenocarcinoma Cells

    Wanjun Yu*, Weidong Peng*, Hanyun Sha, Jipeng Li

    Oncology Research, Vol.27, No.5, pp. 623-628, 2019, DOI:10.3727/096504018X15420734828058

    Abstract Circular RNAs (circRNAs) represent a new class of noncoding RNAs that is involved in the development of cancer. However, little is known about their role in chemoresistance. In the present study, we found that hsa_circ_0003998 expression levels in lung adenocarcinoma (LAD) tissues and docetaxel-resistant cell lines (A549/DTX and H1299/DTX) were upregulated. Knockdown of hsa_circ_0003998 decreased chemoresistance, inhibited proliferation, and enhanced apoptosis in docetaxel-resistant LAD cells. Moreover, by using bioinformatics and luciferase reporter assays, we found that miR-326 was a direct target of hsa_circ_0003998. Functional analysis revealed that miR-326 mediated the effect of hsa_circ_0003998 on chemosensitivity. More >

  • Open Access

    ARTICLE

    XRCC1 Arg399Gln and Arg194Trp polymorphisms regulate XRCC1 expression and chemoresistance of non-small cell lung cancer cells

    Dairong LI1, Xianlu ZHUO1,2, Lumi HUANG1, Xiaohui JI1, Donglin WANG1

    BIOCELL, Vol.43, No.3, pp. 139-144, 2019, DOI:10.32604/biocell.2019.06460

    Abstract X-ray repair cross-complementing protein 1 (XRCC1) could repair cisplatin-induced DNA damage. XRCC1 Arg399Gln and Arg194Trp variants alter XRCC1 expression and function, leading to changes in cancer sensitivity to cisplatin treatment. This study aimed to investigate the effects of XRCC1 Arg399Gln and Arg194Trp polymorphisms on cell viability, apoptosis and XRCC1 expression in cisplatin-sensitive A549 and cisplatin-resistant A549/DDP nonsmall cell lung cancer (NSCLC) cells. Plasmids carrying XRCC1 Arg399Gln and Arg194Trp were constructed and transfected into A549 and A549/DDP cells. RT–PCR, Western blot, MTT assay, and flow cytometry analysis were performed to assess cell viability, apoptosis, and More >

  • Open Access

    ARTICLE

    ClC5 Decreases the Sensitivity of Multiple Myeloma Cells to Bortezomib via Promoting Prosurvival Autophagy

    Huimin Zhang*†, Yuhui Pang, Chuanbao Ma, Jianying Li, Huaquan Wang*, Zonghong Shao*

    Oncology Research, Vol.26, No.3, pp. 421-429, 2018, DOI:10.3727/096504017X15049221237147

    Abstract Resistance to bortezomib (BZ) is the major problem that largely limits its clinical application in multiple myeloma treatment. In the current study, we investigated whether ClC5, a member of the chloride channel family, is involved in this process. The MTT assay showed that BZ treatment decreased cell viability in three multiple myeloma cell lines (ARH77, U266, and SKO-007), with IC50 values of 2.83, 4.37, and 1.91 nM, respectively. Moreover, BZ increased the conversion of LC3B-I to LC3B-II and expressions of beclin-1 and ATG5, concomitantly with a decreased p62 expression. Pharmacological inhibition of autophagy with 3-MA… 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 >

  • Open Access

    ARTICLE

    Overexpression of PER3 Inhibits Self-Renewal Capability and Chemoresistance of Colorectal Cancer Stem-Like Cells via Inhibition of Notch and β-Catenin Signaling

    Feng Zhang*, Hong Sun, Sai Zhang, Xin Yang, Guogang Zhang*, Tao Su

    Oncology Research, Vol.25, No.5, pp. 709-719, 2017, DOI:10.3727/096504016X14772331883976

    Abstract PER3, a circadian clock gene, plays an important role in colorectal cancer, but its action and underlying mechanism in colorectal cancer stem-like cells (CSCs) remain unclear. In this study, the colorectal CSCs were enriched in colorectal HCT-116 sphere-forming cells, expressing lower levels of stem cell markers CD133, CD44, LGR5, and SOX2 compared with HCT-116 cells. A drug-resistant strain from HCT-116 was established. Western blot and qRT-PCR analysis showed that PER3 was downregulated in colorectal CSCs and drug-resistant HCT-116. Overexpression of PER3 could strengthen 5-FU-induced inhibitory effects on colorectal CSCs, but knockdown of PER3 decreased its… More >

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