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Archive > Volume 32 Issue 4 > 2025,32(4):398-404. DOI:10.3872/j.issn.1007-385X.2025.04.008 Prev Next
Basic Research
The effects of lncRNA EBLN3P on the proliferation, migration and epithelial mesenchymal transition (EMT) of thyroid cancer B-CPAP cells by regulating the miR-369-3p/CCND1 axis
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Abstract:
[Abstract] Objective: To investigate the effects of long non-coding RNA (lncRNA) endogenous Bornavirus-like nucleoprotein 3 pseudogene (EBLN3P) on the proliferation, migration and epithelial-mesenchymal transition (EMT) of thyroid cancer B-CPAP cells by regulating the miR-369-3p/CCND1 axis. Methods: 20 samples of thyroid cancer and corresponding adjacent tissue specimens surgically removed at Hainan Cancer Hospital between May 2020 and May 2021, as well as thyroid cancer B-CPAP cells were collected. The levels of EBLN3P, miR-369-3p and CCND1 mRNA in cancer tissues and cells were detected using qPCR and Western blot (WB) methods. The dual-luciferase reporter gene assay was used to validate the targeting relationship among lncRNA EBLN3P, CCND1 and miR-369-3p. B-CPAP cells were randomly divided into the control group, sh-NC group, sh-EBLN3P group, sh-EBLN3P + anti-NC group and sh-EBLN3P + anti-miR-369-3p group. The colony formation assay was used to detect the number of colony formation in each group. The scratch wound healing assay and Transwell assay were performed to evaluate cell migration ability. WB was used to detect the expression of EMT-related proteins. The nude mouse xenograft model of B-CPAP cells was constructed to observe the effect of silencing EBLN3P on the growth of xenograft tumors. Results: The expressions of lncRNA EBLN3P and CCND1 mRNA were up-regulated, and the expression of miR-369-3p was down-regulated in thyroid cancer tissues and B-CPAP cells (all P < 0.05). lncRNA EBLN3P had binding sites with miR-369-3p, and CCND1 had binding sites with miR-369-3p, and there was a targeting relationship. Compared with those in the sh-NC group, the number of clone formation, the scratch healing rate and the number of cell migration in the sh-EBLN3P group decreased (all P < 0.05); the expressions of EBLN3P, CCND1, Ki67, MMP-2, N-cadherin and vimentin was down-regulated; the expressions of miR-369-3p and E-cadherin was up-regulated (all P < 0.05). Compared with those in the sh-EBLN3P + anti-NC group, the expression of miR-369-3p in the sh-EBLN3P + anti-miR-369-3p group was down-regulated; the number of clone formation, scratch healing rate and the number of cell migration increased (all P < 0.05); the expressions of CCND1, Ki67, MMP-2, N-cadherin and vimentin was up-regulated; the expression of E-cadherin was down-regulated (all P < 0.05). Compared with those in the sh-NC group, the volume and weight of B-CPAP cell nude mouse xenograft tumors in the sh-EBLN3P group were significantly reduced (both P < 0.05). Conclusion: The expression of lncRNA EBLN3P is up-regulated in thyroid cancer cells and tissues. Silencing EBLN3P can inhibit the proliferation, migration and EMT of thyroid cancer B-CPAP cells by targeting and regulating the miR-369-3p/CCND1 axis.
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