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- W4280491168 abstract "In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis.Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined.HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3'UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs.This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis." @default.
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- W4280491168 date "2022-05-16" @default.
- W4280491168 modified "2023-10-18" @default.
- W4280491168 title "MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functions in hepatocellular carcinoma by directly targeting hepatoma-derived growth factor HDGF" @default.
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- W4280491168 cites W1992034322 @default.
- W4280491168 cites W1999920543 @default.
- W4280491168 cites W2014610388 @default.
- W4280491168 cites W2029643653 @default.
- W4280491168 cites W2031248889 @default.
- W4280491168 cites W2041509376 @default.
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- W4280491168 cites W2150536104 @default.
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- W4280491168 cites W2155725346 @default.
- W4280491168 cites W2176794756 @default.
- W4280491168 cites W2275678839 @default.
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- W4280491168 cites W2610733803 @default.
- W4280491168 cites W2724336500 @default.
- W4280491168 cites W2757594335 @default.
- W4280491168 cites W2781806573 @default.
- W4280491168 cites W2790573862 @default.
- W4280491168 cites W2795208162 @default.
- W4280491168 cites W2796153225 @default.
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- W4280491168 cites W3135168145 @default.
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- W4280491168 doi "https://doi.org/10.1186/s12935-022-02582-2" @default.
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