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. 2020 Jun 25;13:6073–6083. doi: 10.2147/OTT.S254612

Figure 3.

Figure 3

LATS2 is a direct target of miR-512-3p in HCC. (A) miR-512-3p and its putative binding sequence in the 3ʹUTR of LATS2. The MUT LATS2 binding site was generated in the complementary site for the seed region of miR-512-3p. (B) LATS2 mRNA levels in 45 HCC samples and 45 samples from adjacent normal tissue. p < 0.0001, Student’s t-test. (C) In Pearson’s correlational analysis there was a significant inverse correlation between LATS2 mRNA and miR-512-3p in HCC tissues (r = −0.7785, p < 0.0001). (D) In qRT-PCR analyses LATS2 was significantly downregulated by miR-512-3p at the mRNA level in Hep3B cells and (F) HCCLM3 cells. *p < 0.05, Student’s t-test, n = 3. (E) In Western blot analysis LATS2 was significantly downregulated by miR-512-3p at the protein level in Hep3B cells and (G) HCCLM3 cells. *p < 0.05, Student’s t-test, n = 3. (H) miR-512-3p overexpression significantly suppressed the luciferase activity of WT but not MUT 3ʹUTRs of LATS2. miR-512-3p knockdown caused a dramatic increase in luciferase activity of WT but not MUT 3ʹUTRs of LATS2 in HEK293T cells. *p < 0.05, Student’s t-test, n = 3.