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  • 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

    MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma

    Fang Chen*, Dongqiang Yang, Yuhua Ru, Shan Cao*, Aishe Gao*

    Oncology Research, Vol.27, No.6, pp. 691-701, 2019, DOI:10.3727/096504018X15426763753594

    Abstract Escalating evidence suggests that microRNA-101 (miR-101) is implicated in the development and progression of various cancers, including papillary thyroid carcinoma (PTC). However, the biological function and molecular mechanisms of miR-101 in PTC are still unclear. In this study, we demonstrated that miR-101 expression was significantly decreased in PTC tissues and cell lines. Clinically, a low level of miR-101 was positively associated with advanced histological stages and lymph node and distant metastases. The expression of CXCL12 was negatively correlated with miR-101 level in PTC. CXCL12 was validated as a direct target of miR-101 in PTC cells. More >

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