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<p>Hsa_circ_0002111 is highly expressed in papillary thyroid carcinoma (PTC). We therefore investigated its role and underlying mechanism in promoting PTC progression. Q-RT-PCR, dual-luciferase reporter assays, AGO2-RIP, CCK-8, colony formation, wound healing, and Transwell assays were employed to dissect the circRNA/miRNA/mRNA axis interactions and their functional phenotypes. Results showed that silencing hsa_circ_0002111 significantly inhibited the viability, migration, and invasion of KTC-1 cells. Mechanistic studies demonstrated that hsa_circ_0002111 acted as a sponge for miR-432-5p, which in turn targeted the 3’UTR of CDKN2B and suppressed its expression. Functional assays revealed that either hsa_circ_0002111 knockdown or miR-432-5p overexpression inhibited migration and invasion, whereas inhibition of miR-432-5p reversed these cellular processes. Consistently, siRNA-mediated knockdown of CDKN2B phenocopied the motility defects observed upon hsa_circ_0002111 silencing, suggesting that CDKN2B is a functionally relevant downstream effector. Thus, the hsa_circ_0002111/miR-432-5p/CDKN2B axis is implicated in papillary thyroid carcinoma progression. These findings revealed a novel regulatory mechanism of hsa_circ_0002111 in KTC-1 cells and suggest its potential as a therapeutic target, offering new insights for future clinical applications and research directions in thyroid cancer.</p>

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Hsa_circ_0002111 implicates KTC-1 cell motility and modulates migration and invasion via miR-432-5p/CDKN2B axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Fangyuan Li,
  • Sumei Zhang,
  • Hui Zhu,
  • Ting Xie,
  • Yanlei Yang,
  • Anqi Wang,
  • Dan Guo

摘要

Hsa_circ_0002111 is highly expressed in papillary thyroid carcinoma (PTC). We therefore investigated its role and underlying mechanism in promoting PTC progression. Q-RT-PCR, dual-luciferase reporter assays, AGO2-RIP, CCK-8, colony formation, wound healing, and Transwell assays were employed to dissect the circRNA/miRNA/mRNA axis interactions and their functional phenotypes. Results showed that silencing hsa_circ_0002111 significantly inhibited the viability, migration, and invasion of KTC-1 cells. Mechanistic studies demonstrated that hsa_circ_0002111 acted as a sponge for miR-432-5p, which in turn targeted the 3’UTR of CDKN2B and suppressed its expression. Functional assays revealed that either hsa_circ_0002111 knockdown or miR-432-5p overexpression inhibited migration and invasion, whereas inhibition of miR-432-5p reversed these cellular processes. Consistently, siRNA-mediated knockdown of CDKN2B phenocopied the motility defects observed upon hsa_circ_0002111 silencing, suggesting that CDKN2B is a functionally relevant downstream effector. Thus, the hsa_circ_0002111/miR-432-5p/CDKN2B axis is implicated in papillary thyroid carcinoma progression. These findings revealed a novel regulatory mechanism of hsa_circ_0002111 in KTC-1 cells and suggest its potential as a therapeutic target, offering new insights for future clinical applications and research directions in thyroid cancer.