Long non-coding RNA DUXAP8 promotes the cell proliferation, migration, and invasion of papillary thyroid carcinoma via miR-223-3p mediated regulation of CXCR4

Figures & data

Table 1. The interference sequences of siDUXAP8

Name	Sequences
siDUXAP8#1	CAGCATACTTCAAATTCACAGCAAA
siDUXAP8 #2	AAGATAAAGGTGGTTTCCACAAGAA

Table 2. The sequences of primer

Name	Sequences
lncRNA DUXAP8 F	CACCACAGTTACTTTATCCCTT
lncRNA DUXAP8 R	CCTTTAGACCCATTCTCGTAT
CXCR4 F	CACGCCACCAACAGTCAGA
CXCR4 R	CACAACCACCCACAAGTCA
hsa-miR-223-3p F	TGTCAGTTTGTCAAATACCCC
hsa-miR-223-3p R	GCAGGGTCCGAGGTATTC
β-actin F	CTTAGTTGCGTTACACCCTTTCTTG
β-actin R	CTGTCACCTTCACCGTTCCAGTTT
U6 F U6 R	GCTTCGGCAGCACATATACT GTGCAGGGTCCGAGGTATTC

Figure 1. DUXAP8 expression was upregulated in PTC cell lines and DUXAP8 silencing suppressed PTC cell proliferation. (a) Expression of DUXAP8 in different PTC cell lines. (b-c) Expression of DUXAP8 in GLAG-66 and TPC-1 cells transfected with DUXAP8 siRNAs. (d-e) The proliferation of GLAG-66 and TPC-1 cells was determined by CCK-8 assay. ## p < 0.01, compared to siNC

Figure 2. DUXAP8 silencing inhibited PTC cell migration and invasion. (a-b) The migration ability of GLAG-66 and TPC-1 cells was assessed using a wound-healing assay. (c-d) The invasive capacity of GLAG-66 and TPC-1 cells was detected through the transwell invasion assay. # p < 0.05, ## p < 0.01, compared to siNC

Figure 3. DUXAP8 bound to miR-223-3p and suppressed the expression of miR-223-3p. (a) Sequence alignment of DUXAP8 binding to miR-223-3p. (b) The binding activity between DUXAP8 and miR-223-3p was measured by luciferase reporter assay. ** p < 0.01. (c-d) Expression of miR-223-3p in GLAG-66 and TPC-1 cells was examined using qRT-PCR. ## p < 0.01, compared to siNC

Figure 4. miR-223-3p over-expression inhibited PTC cell proliferation, migration, and invasion. (a-b) CCK-8 assay was performed to examine the proliferation of GLAG-66 and TPC-1 cells. (c-d) A wound-healing assay was carried out to measure GLAG-66 and TPC-1 cell migration. (e-f) The transwell invasion assay was used to assess GLAG-66 and TPC-1 cell invasion. # p < 0.05, ## p < 0.01, compared to NC mimics

Figure 5. CXCR4 was a target of miR-223-3p. (a) Sequence alignment of CXCR4 binding to miR-223-3p. (b) The binding activity between CXCR4 and miR-223-3p was measured by luciferase reporter assay. ** p < 0.01. (c-d) Expression of CXCR4 in GLAG-66 and TPC-1 cells was examined using qRT-PCR. ## p < 0.01, compared to NC mimics

Figure 6. DUXAP8 silencing suppresses PTC cell proliferation, migration, and invasion via the miR-223-3p/CXCR4 axis. (a) The proliferation of GLAG-66 cells was tested using CCK-8. (b-c) The migration activity of GLAG-66 cells was detected by the wound healing assay. (d-e) The invasion of GLAG-66 cells was measured by the transwell invasion assay. # p < 0.05, ## p < 0.01, compared to siDUXAP8 #1

Data availability statement

The data used to support the findings of this study are available from the corresponding author upon request. The supplemenary data were aquired from the database (http://gepia.cancer-pku.cn/detail.php?gene=DUXAP8).