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. 2021 Jun 17;62(7):640–649. doi: 10.3349/ymj.2021.62.7.640

Fig. 2. LINC00662 targeted miR-144-3p in OSCC cells. (A) Bioinformatics analysis was employed for predicting the binding sequence between miR-144-3p and LINC00662. Red-colored letters indicate complementary base pairing. (B and C) The luciferase activity in SCC-9 and ISG15 cells co-transfected with LINC00662-WT or LINC00662-MUT, and miR-control or miR-144-3p mimics was assayed using dual-luciferase reporter gene assay. (D and E) RIP assay was used to validate the direct binding relationship between LINC00662 and miR-144-3p in OSCC cells. (F) qRT-PCR was utilized for quantifying the expression of miR-144-3p in OSCC tissues and adjacent normal tissues. (G) qRT-PCR was used for assaying the expression of miR-144-3p in NOK cells, OSCC cells (SCC-25, ISG15, SCC-9, and CAL-27), and AGS cells. (H) Pearson correlation analysis was employed for evaluating the correlation between miR-144-3p and LINC00662 expression levels in OSCC tissue. (I and J). The expression of LINC00662 or miR-144-3p in SCC-9 and ISG15 cells with LINC00662 overexpression was detected employing qRT-PCR. **p<0.01, ***p<0.001, and NS: p>0.05. WT, wild type; MUT, mutant type; IgG, immunoglobulin G; NOK, normal oral keratinocyte; OSCC, oral squamous cell carcinoma; qRT-PCR, quantitative real-time polymerase chain reaction; RIP, RNA immunoprecipitation; AGS, human gastric adenocarcinoma cell.

Fig. 2