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Search Results (7)
  • Open Access

    ARTICLE

    Cyclin-Dependent Kinase Inhibitor 3 Promotes Cancer Cell Proliferation and Tumorigenesis in Nasopharyngeal Carcinoma by Targeting p27

    Huimin Wang*, Hexin Chen, Hang Zhou*, Wenfa Yu*, Zhenmin Lu*

    Oncology Research, Vol.25, No.9, pp. 1431-1440, 2017, DOI:10.3727/096504017X14835311718295

    Abstract Nasopharyngeal carcinoma (NPC) is a common malignancy of the head and neck that arises from the nasopharynx epithelium and is highly invasive. Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dualspecificity protein phosphatase family, which plays a key role in regulating cell division. Abnormal expression of CDKN3 has been found in numerous types of cancer. In the current study, we explored the possible role of CDKN3 in cell proliferation, ability to invade, and radiosensitivity in NPC cells. We reported that CDKN3 was upregulated and p27 was downregulated in NPC tissues and is associated with a… More >

  • Open Access

    ARTICLE

    Knockdown of Cyclin-Dependent Kinase Inhibitor 3 Inhibits Proliferation and Invasion in Human Gastric Cancer Cells

    Yan Li*, Shan Ji, Li-Ye Fu*, Tao Jiang*, Di Wu*, Fan-Dong Meng*

    Oncology Research, Vol.25, No.5, pp. 721-731, 2017, DOI:10.3727/096504016X14772375848616

    Abstract Cyclin-dependent kinase inhibitor 3 (CDKN3) has been reported to promote tumorigenesis. Since it is unclear whether CDKN3 participates in the development of human gastric cancer, this study assessed the association between CDKN3 expression and cell biological function and demonstrated the clinical significance and prognosis of CDKN3 in human gastric cancer. In this study, we found that CDKN3 showed a high expression in 35 paired human gastric cancer tissues and was correlated with poor patient survival, AJCC clinical staging, and recurrence. Silencing of CDKN3 in human gastric cancer cells can significantly reduce proliferation, migration, invasion, and More >

  • Open Access

    ARTICLE

    3-Methyladenine potentiates paclitaxel-induced apoptosis and phosphorylation of cyclin-dependent kinase 1 at thr161 in nasopharyngeal carcinoma cell

    XIAOQI WU1,2,#, YECHUAN HE1,2,#, YEQIN YUAN4, XIAN TAN1,2, LIN ZHU1,2, DANLING WANG1,2,4, BINYUAN JIANG3,4,*

    BIOCELL, Vol.48, No.5, pp. 861-872, 2024, DOI:10.32604/biocell.2024.048758

    Abstract Background: Nasopharyngeal carcinoma (NPC) exhibits a significant prevalence in the southern regions of China, and paclitaxel (PTX) is frequently employed as a medication for managing advanced NPC. However, drug resistance is typically accompanied by a poor prognosis. Exploring the synergistic potential of combining multiple chemotherapeutic agents may represent a promising avenue for optimizing treatment efficacy. Methods: This study investigated whether 3-Methyladenine (3-MA) could potentiated the effect of PTX and its potential molecular mechanism. Samples were divided into the following categories: Negative control (NC) with the solvent dimethyl sulfoxide (DMSO, 0.5% v/v), PTX (400 nM), 3-MA… More >

  • Open Access

    ARTICLE

    Long non-coding RNA H19 promotes proliferation in hepatocellular carcinoma cells via H19/miR-107/CDK6 axis

    ARCHITTAPON NOKKEAW1,2,3,#, PANNATHON THAMJAMRASSRI1,2,3,#, NAPHAT CHANTARAVISOOT1,4, PISIT TANGKIJVANICH1,2,*, CHAIYABOOT ARIYACHET1,2,*

    Oncology Research, Vol.31, No.6, pp. 989-1005, 2023, DOI:10.32604/or.2023.030395

    Abstract Hepatocellular carcinoma (HCC) is the leading cause of cancer death worldwide; nevertheless, current therapeutic options are limited or ineffective for many patients. Therefore, elucidation of molecular mechanisms in HCC biology could yield important insights for the intervention of novel therapies. Recently, various studies have reported dysregulation of long non-coding RNAs (lncRNAs) in the initiation and progression of HCC, including H19; however, the biological function of H19 in HCC remains unclear. Here, we show that knockdown of H19 disrupted HCC cell growth, impaired the G1-to-S phase transition, and promoted apoptosis, while overexpression of H19 yielded the… More > Graphic Abstract

    Long non-coding RNA H19 promotes proliferation in hepatocellular carcinoma cells via H19/miR-107/CDK6 axis

  • Open Access

    ARTICLE

    MicroRNA-338-3p Inhibits Proliferation and Promotes Apoptosis of Multiple Myeloma Cells Through Targeting Cyclin-Dependent Kinase 4

    Yang Cao*, Xu Shi, Yingmin Liu, Ren Xu§, Qing Ai*

    Oncology Research, Vol.27, No.1, pp. 117-124, 2019, DOI:10.3727/096504018X15213031799835

    Abstract MicroRNA-338-3p (miR-338-3p) has been reported to be a tumor suppressor in multiple cancer types. However, the biological role of miR-338-3p and its underlying mechanism in multiple myeloma (MM) remain unclear. In the present study, we investigated the biological role and potential of miR-338-3p in MM. We found that miR-338-3p was significantly decreased in newly diagnosed and relapsed MM tissues and cell lines. Overexpression of miR-338-3p in MM cells significantly inhibited proliferation and promoted apoptosis, caspase 3, and caspase 8 activity. Bioinformatics algorithm analysis predicted that cyclin-dependent kinase 4 (CDK4) was a direct target of miR-338-3p, More >

  • Open Access

    ARTICLE

    miR-186 Represses Proliferation, Migration, Invasion, and EMT of Hepatocellular Carcinoma via Directly Targeting CDK6

    Junfeng Lu*, Zhongsong Zhao, Yanhong Ma

    Oncology Research, Vol.28, No.5, pp. 509-518, 2020, DOI:10.3727/096504020X15954139263808

    Abstract The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3 -untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its More >

  • Open Access

    ARTICLE

    Anti-proliferative effects of a small molecule inhibitor of CDK AT7519 on chronic myeloid leukemia (CML) cells through halting the transition of cells from G2/M phase of the cell cycle

    MASOUMEH OGHABI1,2, AVA SAFAROGHLI-AZAR1,2, ATIEH POURBAGHERI-SIGAROODI1,2, MOHAMMAD SAYYADI3, MOHSEN HAMIDPOUR1, MOHAMMAD HOSSEIN MOHAMMADI1, DAVOOD BASHASH1,*

    BIOCELL, Vol.44, No.2, pp. 183-192, 2020, DOI:10.32604/biocell.2020.08880

    Abstract Pathogenesis of chronic myeloid leukemia (CML) has mostly been studied with regard to the oncogenic role of BCR/ABL fusion; however, recent disclosures have declared that the challenges with the treatment of CML patients would not be resolved until the role of other aberrancies is ignored. Given the involvement of cyclin-dependent kinases (CDKs) in the pathogenesis of CML, the present study aimed to investigate the effects of a multi-CDK inhibitor AT7519 on BCR/ABL-harboring CML-derived K562 cells. Our results showed that AT7519 effectively reduced the survival of K562 and induced its anti-proliferative effect through the induction of… More >

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