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. 2021 Aug;10(8):3772–3787. doi: 10.21037/tcr-21-1240

Figure 3.

Figure 3

DLX6-AS1 suppressed miR-16-5p expression by direct interaction in NSCLC cells. (A) The complementary binding sites of DLX6-AS1 and miR-16-5p, and mutant sites in DLX6-AS1 MUT reporter. (B,C) DLX6-AS1 WT or DLX6-AS1 MUT reporter was transfected into A549 and H1299 cells along with miR-16-5p mimic or miR-NC, followed by the measurement of luciferase activity at 48 hours upon transfection. (D) A549 and H1299 cells were transfected with miR-16-5p mimic or miR-NC. At 48 hours following transfection, RIP assay and RT-qPCR assay was used to examine the enrichment pattern of DLX6-AS1 in IgG or AGO2 IP complex. (E) The RT-qPCR assay was performed to detect miR-16-5p expression in 16HBE, A549, and H1299 cells. (F,G) A549 and H1299 cells were transfected with pcDNA, pcDNA-DLX6-AS1, si-NC, or si-DLX6-AS1, respectively. DLX6-AS1 and miR-16-5p level were subsequently measured by RT-qPCR assay at 48 hours after transfection. *, P<0.05. DLX6-AS1, distal-less homeobox 6 antisense RNA 1; miR-16-5p, microRNA-16-5p; NSCLC, non-small cell lung cancer; MUT, mutant-type; WT, wide-type; RIP, RNA immunoprecipitation; RT-qPCR, reverse transcription-quantitative PCR.