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

ABSTRACT

Papillary thyroid carcinoma (PTC) is a differentiated type of thyroid malignancy with a high incidence. Long non-coding RNA (lncRNA) DUXAP8 has been reported to participate in the proliferation, migration, and invasion of several cancer types. However, its association with PTC has not yet been reported. The current study aimed to investigate the role of DUXAP8 in PTC and revealed the underlying mechanisms. The expression of DUXAP8 was knocked down in two PTC cell lines and the effects of DUXAP8 on the PTC biological behavior were examined by cell counting kit-8 (CCK-8), wound healing, and transwell invasion assays. Luciferase reporter assay was used to detect the binding activity between miR-223-3p and DUXAP8. We found that knockdown of DUXAP8 inhibited the proliferation, migration, and invasion of PTC cells. DUXAP8 could sponge miR-223-3p through the specific binding site. CXCR4 was a target of miR-223-3p. The malignant phenotypes of the PTC cells were suppressed by the over-expression of miR-223-3p. Moreover, miR-223-3p inhibition or CXCR4 over-expression partly restored the proliferation, migration, and invasion activities of DUXAP8-downregulated PTC cells. The results evidenced that DUXAP8 acted as an oncogene in PTC, these effects seemed to partly dependent on the miR-223-3p/CXCR4 axis.

Graphical abstract

KEYWORDS:

• Papillary thyroid carcinoma
• long non-coding RNA DUXAP8
• miR-223-3p
• CXCR4
• proliferation
• migration and invasion

Research highlights

• DUXAP8 silencing suppressed PTC cell proliferation, migration, and invasion

• DUXAP8 bound to miR-223-3p and reduced the expression of miR-223-3p

• The miR-223-3p suppressed the PTC cell proliferation, migration, and invasion

• DUXAP8 promoted PTC progression via the miR-223-3p/CXCR4 axis

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).

Disclosure statement

The authors have no conflicts of interest to declare.

Supplementary material

Supplemental data for this article can be accessed here.

Additional information

Funding

This research was funded by the “13th Five-Year” Science and Technology Project of Jilin Provincial Education Department—JJKH20201092KJ.