Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (4)
  • Open Access

    ARTICLE

    UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer by Sponging miR-135a

    Xiaobo Zhang*, Feng Gao*, Lei Zhou*, Huaitao Wang*, Gang Shi, Xiaodong Tan*

    Oncology Research, Vol.25, No.9, pp. 1529-1541, 2017, DOI:10.3727/096504017X14888987683152

    Abstract Pancreatic cancer (PC) is a devastating malignant disease with a poor prognosis. This study aimed to investigate the role of urothelial carcinoma associated 1 (UCA1) in the progression of PC. Our results revealed that long noncoding RNA (lncRNA) UCA1 was overexpressed in PC tissues compared with adjacent histologically normal tissues. A downregulated level of UCA1 was also detected in five human PC cell lines (SW1990, BxPC-3, MiaPaCa-2, PANC-1, and CAPAN-1) compared with normal pancreatic duct epithelial HPDE cells. The proliferation of PC cells was inhibited after UCA1 was suppressed by a lentiviral vector. The cell… More >

  • Open Access

    ARTICLE

    Long Noncoding RNA GAS5 Inhibits Tumorigenesis and Enhances Radiosensitivity by Suppressing miR-135b Expression in Non-Small Cell Lung Cancer

    Yingbo Xue, Tingting Ni, Ying Jiang, Yong Li

    Oncology Research, Vol.25, No.8, pp. 1305-1316, 2017, DOI:10.3727/096504017X14850182723737

    Abstract Growth arrest-specific transcript 5 (GAS5) has been demonstrated to correlate with clinicopathological characteristics and serve as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the underlying mechanism of the competing endogenous RNA (ceRNA) regulatory network involving GAS5 in NSCLC remains to be elucidated. In this study, qRT-PCR results showed that GAS5 was downregulated and miR-135b was upregulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely in response to irradiation. Gain-of-function experiments revealed that GAS5 overexpression and miR-135b downregulation significantly suppressed tumorigenesis by repressing cell proliferation and invasion, and 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

    Downregulation of MicroRNA-135 Promotes Sensitivity of Non-Small Cell Lung Cancer to Gefitinib by Targeting TRIM16

    Ning Wang*1, Tingting Zhang†1

    Oncology Research, Vol.26, No.7, pp. 1005-1014, 2018, DOI:10.3727/096504017X15144755633680

    Abstract Personalized treatment targeting the epidermal growth factor receptor (EGFR) may be a promising new treatment of non-small cell lung cancer (NSCLC). Gefitinib, a tyrosine kinase inhibitor, is the first drug for NSCLC, which unfortunately easily leads to drug resistance. Our study aimed to explore the functional role of microRNA (miR)-135 in the sensitivity to gefitinib of NSCLC cells. Expression of miR-135 in normal cells and NSCLC cells was assessed, followed by the effects of abnormally expressed miR-135 on cell viability, migration, invasion, apoptosis, sensitivity to gefitinib, and the expression levels of adhesion molecules and programmed… More >

Displaying 1-10 on page 1 of 4. Per Page