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The overexpression of PTEN concomitant with Livin gene silencing was confirmed as a feasible and effective in vitro and in vivo gene modulation method, which may represent a potential therapeutic strategy for the treatment of Gastric Cancer.
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Livin overexpression not only significantly inhibited RCC cell apoptosis and increased cell viability, but completely reversed the si-CCAT1-mediated repression of cell viability
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our results revealed that Livin induced EMT through the activation of the p38/GSK3beta pathway, which in turn promoted the progression and metastasis of breast cancer, especially for triple-negative breast cancer (TNBC)
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our results suggest that siRNA-mediated Livin knockdown enhanced the chemosensitivity of the three head and neck squamous cell carcinoma cell lines to cisplatin, 5-FU and docetaxel.
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Livin is specifically over-expressed in adrenocortical carcinoma.
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Further experiments confirmed the induction of cell apoptosis and suppression of cell proliferation by anti-MM scFv-tP in LiBr cells, along with efficient silence of Livin gene both in vitro and in vivo. Altogether, our findings provide a feasible approach to transport Livin small interfering RNA to malignant melanoma cells which would be a new therapeutic strategy for combating malignant melanoma
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MicroRNA-214 inhibits the osteogenic differentiation of human osteoblasts through the direct regulation of BIRC7.
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the results of the present study suggested that Livin may enhance tumorigenesis by modulating the mitogenactivated/Akt signaling pathways in human HSCC.
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Positive BIRC7 expression and negative KLF4 expression are associated with the progression of PDAC and poor prognosis in patients with PDAC.
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High expression of BIRC7 is associated with drug resistance in Renal cell carcinoma.
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Data show that cylindromatosis (CYLD) overexpression and livin knockdown might improve gemcitabine chemosensitivity by decreasing autophagy and increasing apoptosis in bladder cancer (BCa) cells.
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The apoptosisinducing effects of livin and surivin knockdown were investigated using a Hoechst staining kit.
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Expression of livin, survivin and caspase-3 are closely related to the occurrence and development of prostatic cancer.
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Our results suggested the important role of Livin and its partner molecule in the process of VSV treatment
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Data showed that Livin knock-down suppressed cell proliferation and inhibited cell invasion, accompanied by downregulation of VEGF and MMP-2/-9. Its silencing resulted in the prevention of xenograft tumor formation.
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These findings suggest that livin may be used as a novel target for tumor gene therapy.
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Upregulation of Livin expression and downregulation of caspase activity are observed under cycling and chronic hypoxia in glioblastoma cells and xenografts.
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Livin expression was higher in condyloma acuminatum than in normal cells and was correlated with survivin and Ki-67.
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Livin gene has a high expression in osteosarcoma and inhibits apoptosis in tumor tissue.
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livin is associated with invasive and oncogenic phenotypes such as tumor cell invasion, tumor cell migration, tumor cell proliferation, and resistance to apoptosis in human oral squamous cell carcinoma cells.
