Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (23)
  • Open Access

    ARTICLE

    miR-4792 Inhibits Acute Myeloid Leukemia Cell Proliferation and Invasion and Promotes Cell Apoptosis by Targeting Kindlin-3

    Yun Qin*, Yu Wang†‡§, Dongbo Liu

    Oncology Research, Vol.28, No.4, pp. 357-369, 2020, DOI:10.3727/096504020X15844389264424

    Abstract It has been reported that kindlin-3 expression is closely associated with progression of many cancers and microRNA (miRNA) processing. However, the effects and precise mechanisms of kindlin-3 in acute myeloid leukemia (AML) have not been well clarified. Our study aimed to explore the interaction between kindlin-3 and miR-4792 in AML. In our study, we found that the expression of kindlin-3 was dramatically increased in AML samples and cell lines, and the miR-4792 level was significantly downregulated. Interestingly, the low miR-4792 level was closely associated with upregulated kindlin-3 expression in AML samples. Moreover, introduction of miR-4792 More >

  • Open Access

    CORRECTION

    Kallistatin Suppresses Cell Proliferation and Invasion and Promotes Apoptosis in Cervical Cancer Through Blocking NF-κB Signaling

    Tao Wang, Fan Shi, JiQuan Wang, Zi Liu, Jin Su

    Oncology Research, Vol.28, No.9, pp. 969-970, 2020, DOI:10.3727/096504022X16414984936773

    Abstract Kallistatin has been recognized as an endogenous angiogenesis inhibitor and exerts pleiotropic effects in inhibiting tumor growth, migration, apoptosis, and inflammation. The purpose of the present study was to investigate the potential role and mechanisms of kallistatin in cervical cancer. We demonstrated that kallistatin effectively inhibited cell proliferation and enhanced apoptosis in a dose-dependent manner. Additionally, kallistatin suppressed migration and invasion activities and markedly reduced the expression of matrix-degrading metalloproteinases, progelatinase (MMP-2), MMP-9, and urokinase-type PA (uPA). Kallistatin reversed the epithelial–mesenchymal transition (EMT) and caused the upregulation of epithelial markers such as E-cadherin and inhibited… More >

  • Open Access

    CORRECTION

    MicroRNA-139-5p Inhibits Cell Proliferation and Invasion by Targeting RHO-Associated Coiled-Coil-Containing Protein Kinase 2 in Ovarian Cancer

    Yanli Wang*, Jia Li, Chunling Xu, Xiaomeng Zhang

    Oncology Research, Vol.28, No.7-8, pp. 823-825, 2020, DOI:10.3727/096504021X16240202940021

    Abstract Increasing evidence indicates that the dysregulation of microRNAs is associated with the development and progression of various cancers. MicroRNA-139-5p (miR-139-5p) has been reported to have a tumor suppressive role in many types of cancers. The role of miR-139-5p in ovarian cancer (OC) is poorly understood. The purpose of the present study was to explore the expression of miR-139-5p and its function in OC. The results showed that miR-139-5p expression was markedly downregulated in OC tissues and cell lines. In addition, underexpression of miR-139-5p was significantly associated with FIGO stage, lymph mode metastasis, and poor overall… More >

  • Open Access

    ARTICLE

    miR-363-3p Inhibits Osteosarcoma Cell Proliferation and Invasion via Targeting SOX4

    Kejun Wang*1, Lin Yan*1, Fen Lu

    Oncology Research, Vol.27, No.2, pp. 157-163, 2019, DOI:10.3727/096504018X15190861873459

    Abstract miR-363-3p has been shown to suppress tumor growth and metastasis in various human cancers. However, the function of miR-363-3p in osteosarcoma (OS) has not been determined. In our study, we found that the expression of miR-363-3p was significantly downregulated in OS tissues compared with adjacent normal tissues. miR-363-3p expression was associated with the poor overall survival rate of OS patients. Moreover, we found that overexpression of miR-363-3p markedly inhibited the proliferation, migration, and invasion of U2OS and MG63 cells. Moreover, we found that SOX4 was a direct target of miR-363-3p in OS cells. Overexpression of More >

  • Open Access

    ARTICLE

    Overexpression of miR-1283 Inhibits Cell Proliferation and Invasion of Glioma Cells by Targeting ATF4

    Hao Chen, Yi Zhang, Hai Su, Hui Shi, Qijiang Xiong, Zulu Su

    Oncology Research, Vol.27, No.3, pp. 325-334, 2019, DOI:10.3727/096504018X15251282086836

    Abstract It is well known that activating transcription factor 4 (ATF4) expression is closely associated with progression of many cancers. We found that miR-1283 could directly target ATF4. However, the precise mechanisms of miR-1283 in glioma have not been well clarified. Our study aimed to explore the interaction between ATF4 and miR-1283 in glioma. In this study, we found that the level of miR-1283 was dramatically decreased in glioma tissues and cell lines, the expression of ATF4 was significantly increased, and the low level of miR-1283 was closely associated with high expression of ATF4 in glioma More >

  • Open Access

    ARTICLE

    miR-615 Inhibits Prostate Cancer Cell Proliferation and Invasion by Directly Targeting Cyclin D2

    Fengyu Huang*†, Hongjun Zhao, Zhaojin Du, Hong Jiang§

    Oncology Research, Vol.27, No.3, pp. 293-299, 2019, DOI:10.3727/096504018X15190399381143

    Abstract Previous studies have reported that miR-615 exerts a tumor suppressor role in some tumors, such as esophageal squamous cell carcinoma and non-small cell lung cancer. However, the role of miR-615 in prostate cancer has not been defined. Here we found that miR-615 was downregulated in prostate cancer tissues and cell lines. Overexpression of miR-615 in PC-3 cells significantly inhibited cellular proliferation, migration, and invasion. Moreover, overexpression of miR-615 delayed tumor growth in vivo. In terms of mechanism, we found that cyclin D2 (CCND2) is a target gene of miR-615 in prostate cancer. We showed that More >

  • Open Access

    ARTICLE

    NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1b/NF-kB p65 Signals

    Liping Xue*1, Bin Lu†1, Bibo Gao, Yangyang Shi, Jingqi Xu, Rui Yang, Bo Xu, Peng Ding

    Oncology Research, Vol.27, No.5, pp. 557-564, 2019, DOI:10.3727/096504018X15264647024196

    Abstract Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1 , IL-1 antibody, and NF- B inhibitor.… More >

  • Open Access

    ARTICLE

    MicroRNA-598 Inhibits Cell Proliferation and Invasion of Glioblastoma by Directly Targeting Metastasis Associated in Colon Cancer-1 (MACC1)

    Ning Wang*1, Yang Zhang†1, Huaxin Liang

    Oncology Research, Vol.26, No.8, pp. 1275-1283, 2018, DOI:10.3727/096504018X15185735627746

    Abstract The dysregulation of microRNA (miRNA) expression is closely related with tumorigenesis and tumor development in glioblastoma (GBM). In this study, we found that miRNA-598 (miR-598) expression was significantly downregulated in GBM tissues and cell lines. Restoring miR-598 expression inhibited cell proliferation and invasion in GBM. Moreover, we validated that metastasis associated in colon cancer-1 (MACC1) is a novel target of miR-598 in GBM. Restoring MACC1 expression reversed the inhibitory effects of miR-598 overexpression on GBM cells. In addition, miR-598 overexpression suppressed Met/ AKT pathway activation in GBM. Our results provided compelling evidence that miR-598 serves More >

  • Open Access

    ARTICLE

    MicroRNA-379 Suppresses Cervical Cancer Cell Proliferation and Invasion by Directly Targeting V-crk Avian Sarcoma Virus CT10 Oncogene Homolog-Like (CRKL)

    Xi Shi*1, Xiao Xiao†1, Na Yuan*, Shili Zhang*, Fukang Yuan, Xiaohong Wang§

    Oncology Research, Vol.26, No.7, pp. 987-996, 2018, DOI:10.3727/096504017X15140534417184

    Abstract Cervical cancer is the fourth most common malignancy among females worldwide. MicroRNA-379 (miR-379) is aberrantly expressed in multiple human cancer types. However, the expression pattern, roles, and detailed regulatory mechanisms of miR-379 in cervical cancer remain unknown. In this study, we found that miR-379 expression was downregulated in cervical cancer tissues and cell lines. Low miR-379 expression was correlated with International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and distant metastasis. Additionally, miR-379 overexpression suppressed the proliferation and invasion of cervical cancer cells. Furthermore, V-crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) More >

  • Open Access

    ARTICLE

    miR-204 Regulates Cell Proliferation and Invasion by Targeting EphB2 in Human Cervical Cancer

    Shanhong Duan*, Ali Wu, Zhengyu Chen, Yarong Yang*, Liying Liu*, Qi Shu*

    Oncology Research, Vol.26, No.5, pp. 713-723, 2018, DOI:10.3727/096504017X15016337254641

    Abstract MicroRNAs (miRNAs) are small noncoding RNAs that are involved in human carcinogenesis and progression. miR-204 has been reported to be a tumor suppressor in several cancer types. However, the function and underlying molecular mechanism of miR-204 in cervical cancer (CC) are still unclear. In the present study, the expression level of miR-204 was measured using the qRT-PCR method in 30 paired CC clinical samples and in 6 CC cell lines. We found that the expression of miR-204 was significantly downregulated in CC tissues and cell lines compared to normal cervical tissues and cell line. miR-204… More >

Displaying 1-10 on page 1 of 23. Per Page