Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (5)
  • Open Access

    RETRACTION

    Retraction: Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

    Oncology Research Editorial Office

    Oncology Research, Vol.32, No.8, pp. 1381-1381, 2024, DOI:10.32604/or.2024.055035 - 17 July 2024

    Abstract This article has no abstract. More >

  • Open Access

    ARTICLE

    Hepatitis B virus X protein-mediated upregulation of miR-221 activates the CXCL12-CXCR4 axis to promote NKT cells in HBV-related hepatocellular carcinoma

    YUE CAO, LIN HU, YISHU TANG*

    BIOCELL, Vol.47, No.7, pp. 1537-1548, 2023, DOI:10.32604/biocell.2023.027205 - 21 June 2023

    Abstract Backgrounds: Both hepatitis B virus X protein (HBx) and microRNA-221 (miR-221) have been implicated in the development of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). The present study demonstrates that HBx promotes HCC cell proliferation via the C-X-C motif chemokine ligand 12-C-X-C chemokine receptor type 4 (CXCL12-CXCR4) axis. We predict that HBx/miR-221-mediated CXCL12/CXCR4 signaling induces NKT cells to promote HBV-related HCC. Methods: After miR-221 mimic, miR-221 mimic negative control, miR-221 inhibitor, miR-221 inhibitor negative control were transfected into cells, the expression of CXCL12 and miR-221 was detected by qPCR and western blot. Then we constructed… More >

  • Open Access

    ARTICLE

    A549/DDP derived exosomes can affect cisplatin chemosensitivity via transporting CXCR4 to A549 cells

    MINGMING FANG1,#, NING GE2,#, JIANFANG LIU3,*, YAYUN CUI2,*

    BIOCELL, Vol.46, No.3, pp. 711-720, 2022, DOI:10.32604/biocell.2022.016714 - 18 November 2021

    Abstract The resistance of cancer cells to the anti-cancer drugs is the most important reason that affecting the efficacy of the non-small cell lung cancer (NSCLC) chemotherapy; thus, to explore the underlying mechanism of drug resistance of NSCLC medications is urgently needed for improving the therapeutic efficacy of current anti-NSCLC chemotherapies. The aim of the present study is to explore the roles of exosomes in the chemosensitivity of A549 cells and the related mechanism. A549 cells and cisplatin resistant cell line A549/DDP derived exosomes were isolated, and the expressions of CXCR4 were compared. Then, after cisplatin… More >

  • Open Access

    ARTICLE

    Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

    Genglong Zhu*, Xialei Liu*, Yonghui Su, Fangen Kong, Xiaopeng Hong*, Zhidong Lin

    Oncology Research, Vol.27, No.1, pp. 55-64, 2019, DOI:10.3727/096504018X15201143705855

    Abstract Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of… More >

  • Open Access

    ARTICLE

    Long Noncoding RNA GAS5 Promotes Proliferation, Migration, and Invasion by Regulation of miR-301a in Esophageal Cancer

    Wei Li, Weidong Zhao, Zhaohui Lu, Wen Zhang, Xuan Yang

    Oncology Research, Vol.26, No.8, pp. 1285-1294, 2018, DOI:10.3727/096504018X15166193231711

    Abstract Long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) has been revealed to be associated with the progression of various cancers. However, the biological roles of GAS5 in esophageal cancer (EC) remain unclear. We aimed to thoroughly explore the functions of GAS5 in EC. The results showed that GAS5 expression was increased in EC cells (ECA109, TE-1, TE-3, and EC9706) compared to SHEE cells. Knockdown of GAS5 decreased cell viability, migration, and invasion and induced apoptosis in EC9706 cells. Moreover, miR-301a appeared to be directly sponged by GAS5, and miR-301a suppression obviously alleviated the protumor More >

Displaying 1-10 on page 1 of 5. Per Page