Lnc-CTSLP4 inhibits EMT via suppressing HNRNPAB-mediated Snail transcriptional activation in GC cells
(A) The expression level of E-cadherin, N-cadherin, HNRNPAB, and Snail in MGC803 and HGC27 cells after shRNA knockdown (sh-HNRNPAB) or overexpression (HNRNPAB) of HNRNPAB (∗∗p < 0.01, ∗∗∗p < 0.001). (B) The binding of HNRNPAB to the Snail promoter in GC cells (ChIP-PCR assays, ∗∗p < 0.01, ∗∗∗p < 0.001). (C and D) pGL3-Basic-SNAIL and pGL3-Basic-SNAIL-del (deletion at position −866 to −862 bp) constructs, along with the pRL-TK plasmid, were transfected into HGC27-HNRNPAB cells and HGC27-Vector cells, and then the relative luciferase activity was measured (∗∗p < 0.01, ∗∗∗p < 0.001). (E and F) Western blot (E) and densitometric analysis (F) of E-cadherin, N-cadherin, HNRNPAB, and Snail in MGC803 and AGS cells transfected with AV-CTSLP4, HNRNPAB-expressing vector, or Snail si-RNA (∗∗p < 0.01, ∗∗∗p < 0.001).