Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (37)
  • Open Access

    ARTICLE

    The NAC Transcription Factor ANAC089 Modulates Seed Vigor through the ABI5-VTC2 Module in Arabidopsis thaliana

    Yuan Tian, Lulu Zhi, Ping Li*, Xiangyang Hu*

    Phyton-International Journal of Experimental Botany, Vol.93, No.6, pp. 1101-1116, 2024, DOI:10.32604/phyton.2024.050220

    Abstract Seed viability is an essential feature for genetic resource conservation as well as sustainable crop production. Long-term storage induces seed viability deterioration or seed aging, accompanied by the accumulation of toxic reactive oxygen species (ROS) to suppress seed germination. Controlled deterioration treatment (CDT) is a general approach for mimicking seed aging. The transcription factor ANAC089 was previously reported to modulate seed primary germination. In this study, we evaluated the ability of ANAC089 to control seed viability during aging. Compared with that in the wild-type line, the mutation of ANAC089 significantly increased HO, thereby reducing seed viability after… More >

  • Open Access

    ARTICLE

    Knockdown of HPIP Inhibits the Proliferation and Invasion of Head-and-Neck Squamous Cell Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway

    Yangjing Chen, Ruimin Zhao, Qian Zhao, Yuan Shao, Shaoqiang Zhang

    Oncology Research, Vol.24, No.3, pp. 153-160, 2016, DOI:10.3727/096504016X14612603423476

    Abstract Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a corepressor for the transcription factor PBX. Previous studies showed that HPIP is frequently overexpressed in many tumors. However, the role of HPIP in head-and-neck squamous cell carcinoma (HNSCC) has not yet been determined. Thus, we decided to investigate the effects and mechanisms of HPIP in HNSCC. Our results demonstrated that HPIP is highly expressed in human HNSCC cell lines and provides the first evidence that knockdown of HPIP obviously inhibits proliferation and migration/invasion in HNSCC cells in vitro, as well as inhibits tumor growth in More >

  • Open Access

    ARTICLE

    miR-34b Targets HSF1 to Suppress Cell Survival in Acute Myeloid Leukemia

    Gangcan Li, Yanping Song, Yunjie Zhang, Hao Wang, Jia Xie

    Oncology Research, Vol.24, No.2, pp. 109-116, 2016, DOI:10.3727/096504016X14611963142254

    Abstract Acute myeloid leukemia (AML) is the most lethal hematological malignancy, and the occurrence of chemoresistance prevents the achievement of complete remission following the standard therapy. MicroRNAs have been extensively investigated as critical regulators of hematopoiesis and leukemogenesis, and they represent a promising strategy for AML therapy. In this study, we identified miR-34b as a novel regulator in myeloid proliferation and apoptosis of leukemic cells. We found that miR-34b was developmentally upregulated in plasma and myeloid cells of healthy subjects, while it was significantly reduced in blood samples of patients with AML and AML cell lines.… More >

  • Open Access

    ARTICLE

    Overexpression of T-box Transcription Factor 5 (TBX5) Inhibits Proliferation and Invasion in Non-Small Cell Lung Carcinoma Cells

    Ruoting Ma*†, Yu Yang*, Qiuyun Tu, Ke Hu

    Oncology Research, Vol.25, No.9, pp. 1495-1504, 2017, DOI:10.3727/096504017X14883287513729

    Abstract T-box transcription factor 5 (TBX5), a member of the conserved T-box transcription factor family that functions in organogenesis and embryogenesis, has recently been identified as a critical player in cancer development. The aim of this study was to determine the role of TBX5 in non-small cell lung carcinoma (NSCLC). Immunohistochemistry was used to detect the correlation between levels of TBX5 and clinicopathological features of NSCLC patients in tissue microarray. Expression of TBX5 in NSCLC tissues and cell lines was evaluated by quantitative PCR and Western blot. The role of TBX5 in regulating proliferation, colony formation,… More >

  • Open Access

    ARTICLE

    Basic Transcription Factor 3 Is Required for Proliferation and Epithelial–Mesenchymal Transition via Regulation of FOXM1 and JAK2/STAT3 Signaling in Gastric Cancer

    De-Zhong Zhang*, Bing-He Chen*, Lan-Fang Zhang, Ming-Kun Cheng, Xiang-Jie Fang*, Xin-Jun Wu*

    Oncology Research, Vol.25, No.9, pp. 1453-1462, 2017, DOI:10.3727/096504017X14886494526344

    Abstract Gastric cancer (GC) is the most common epithelial malignancy worldwide. Basic transcription factor 3 (BTF3) plays a crucial role in the regulation of various biological processes. We designed experiments to investigate the molecular mechanism underlying the role of BTF3 in GC cell proliferation and metastasis. We confirmed that BTF3 expression was decreased in GC tissues and several GC cell lines. Lentivirus-mediated downregulation of BTF3 reduced cell proliferation, induced S and G2/M cell cycle arrest, and increased apoptosis. Knockdown of BTF3 significantly reduced the expression of Forkhead box M1 (FOXM1). Upregulation of FOXM1 significantly inhibited the decrease… More >

  • Open Access

    ARTICLE

    miR-365 Suppresses Cholangiocarcinoma Cell Proliferation and Induces Apoptosis by Targeting E2F2

    Lunjian Chen*, Xiaorong Huang, Xinxin Chen

    Oncology Research, Vol.26, No.9, pp. 1375-1382, 2018, DOI:10.3727/096504018X15188352857437

    Abstract Cholangiocarcinoma (CCA) is one of the most malignant adenocarcinomas arising from bile duct epithelial cells. However, the molecular mechanism regulating CCA development and progression still needs to be investigated. Here we found that miR-365 was downregulated in CCA tissues compared with adjacent normal tissues. By functional experiments, we found that overexpression of miR-365 significantly inhibited CCA cell proliferation and promoted cellular apoptosis in vitro. Furthermore, administration with miR-365 markedly suppressed the growth of tumor tissues in vivo. Mechanistically, we identified E2F2 as the target gene of miR- 365 in CCA cells. We found that overexpression More >

  • Open Access

    ARTICLE

    Let-7c Inhibits the Proliferation, Invasion, and Migration of Glioma Cells via Targeting E2F5

    Mengyi Huang, Xin Gong

    Oncology Research, Vol.26, No.7, pp. 1103-1111, 2018, DOI:10.3727/096504018X15164123839400

    Abstract As a member of the miRNA family, let-7c has been identified as a tumor suppressor in many cancers. However, the molecular biological function of let-7c in glioma has not been elucidated. The aim of this study was to explore let-7c expression levels and evaluate its function in glioma cells. We first measured the expression of let-7c in four glioma cell lines and a normal cell line by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), and the results showed that let-7c was downregulated in glioma cells. By applying gain-of-function and loss-of-function assays, the experiments suggested More >

  • Open Access

    ARTICLE

    T-box Transcription Factor Tbx3 Contributes to Human Hepatocellular Carcinoma Cell Migration and Invasion by Repressing E-Cadherin Expression

    Xianguang Feng*, Wenhuan Yao, Zengzhen Zhang*, Fangshui Yuan*, Li Liang*, Jingqiang Zhou*, Shuang Liu*, Jiqing Song

    Oncology Research, Vol.26, No.6, pp. 959-966, 2018, DOI:10.3727/096504017X15145624664031

    Abstract Tbx3, a member of the T-box family of transcription factors, contributes directly to tumor formation, migration, and invasion. However, the role of Tbx3 in the metastasis of HCC remains unclear. In the present study, Tbx3 expression was detected in HCC tissues and cells by Western blot, and Tbx3 expression was regulated by use of siRNAs or lentivirus-mediated vectors. Here we found that Tbx3 protein expression increased in HCC tissues and cell lines. Tbx3 expression was positively associated with multiple tumor nodes, venous infiltration, and advanced TNM tumor stage. Survival analysis demonstrated that Tbx3 expression was… More >

  • Open Access

    ARTICLE

    MicroRNA-152 Suppresses Human Osteosarcoma Cell Proliferation and Invasion by Targeting E2F Transcription Factor 3

    Chao Ma, Jinfeng Han, Dong Dong, Nanya Wang

    Oncology Research, Vol.26, No.5, pp. 765-773, 2018, DOI:10.3727/096504017X15021536183535

    Abstract MicroRNA-152 (miR-152) expression has been reported to be downregulated in osteosarcoma (OS). However, the role of miR-152 in OS is not well documented. In the present study, we aimed to explore the function and underlying mechanism of miR-152 in OS. We found that miR-152 was underexpressed in OS tissues and cell lines. Decreased miR-152 was inversely correlated with lymph node metastasis and advanced clinical stage. Overexpression of miR-152 significantly inhibited cell proliferation, colony formation, migration, and invasion of OS cells. Bioinformatics analyses showed that miR-152 directly targeted E2F transcription factor 3 (E2F3), as further confirmed More >

  • Open Access

    ARTICLE

    miR-144-3p Targets FosB Proto-oncogene, AP-1 Transcription Factor Subunit (FOSB) to Suppress Proliferation, Migration, and Invasion of PANC-1 Pancreatic Cancer Cells

    Shidan Liu1, Jiaxi Luan1, Yan Ding

    Oncology Research, Vol.26, No.5, pp. 683-690, 2018, DOI:10.3727/096504017X14982585511252

    Abstract This study aimed to investigate the role of miR-144-3p in pancreatic cancer (PC) carcinogenesis and to explore the mechanism of its function in PC. miR-144-3p was downregulated in PC tissues and cells. miR-144-3p overexpression significantly inhibited PC cell proliferation, migration, and invasion. FosB proto-oncogene, AP-1 transcription factor subunit (FOSB) was a target gene of miR-144-3p. miR-144-3p could repress PC cell proliferation, migration, and invasion by inhibiting the expression of FOSB. In conclusion, miR-144-3p plays an important role in PC cell proliferation, migration, and invasion by targeting FOSB. miR-144-3p may provide a new target for the More >

Displaying 1-10 on page 1 of 37. Per Page