Research Paper Volume 13, Issue 12 pp 16267—16286

Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A

Overexpression of DNMT3A promotes hepatocellular carcinoma cell progression weakened by miR-29b-3p or sh-HCP5. (A) Hep3B and HCCLM3 cells with up-regulation of miR-29b-3p or knockdown of HCP5 and that were transfected with NC or DNMT3A up-regulated plasmid (DNMT3A-OV) were evaluated by qRT-PCR (*pB) The expression of DNMT3A in Hep3B and HCCLM3 cell lines transfected with NC or DNMT3A-OV examined by Western blot analysis for miR-29b-3p overexpression or HCP5 knockdown (*pC) The cell proliferation rate increases when treated with DNMT3A-OV (*pD, E) DNMT3A promotes the cell metastatic and invasive capacity (*pF) DNMT3A promotes cell proliferation through inhibiting cell apoptosis (*pG) DNMT3A promotes epithelial-mesenchymal transition (EMT) progress by increasing E-cadherin and decreasing vimentin.

Figure 8. Overexpression of DNMT3A promotes hepatocellular carcinoma cell progression weakened by miR-29b-3p or sh-HCP5. (A) Hep3B and HCCLM3 cells with up-regulation of miR-29b-3p or knockdown of HCP5 and that were transfected with NC or DNMT3A up-regulated plasmid (DNMT3A-OV) were evaluated by qRT-PCR (*p<0.05). (B) The expression of DNMT3A in Hep3B and HCCLM3 cell lines transfected with NC or DNMT3A-OV examined by Western blot analysis for miR-29b-3p overexpression or HCP5 knockdown (*p<0.05). (C) The cell proliferation rate increases when treated with DNMT3A-OV (*p<0.05). (D, E) DNMT3A promotes the cell metastatic and invasive capacity (*p<0.05). (F) DNMT3A promotes cell proliferation through inhibiting cell apoptosis (*p<0.05). (G) DNMT3A promotes epithelial-mesenchymal transition (EMT) progress by increasing E-cadherin and decreasing vimentin.