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<p>Recently, a novel circular RNA (circRNA), circPTP4A2 (hsa_circ_0007364), was reported to promote cervical cancer progression. However, its specific role in non-small cell lung cancer (NSCLC) remains unclear. Here, we observed that circPTP4A2 is significantly upregulated in NSCLC tissues and cell lines. Furthermore, multivariate Cox proportional hazards regression analysis confirmed that high circPTP4A2 expression is independently associated with poor prognosis in NSCLC patients after adjusting for confounding clinicopathological covariates. Knockdown of circPTP4A2 significantly suppressed the proliferation, migration, and invasion capabilities of H1299 and A549 cells. Additionally, we identified miR-183-5p as a direct targeted of circPTP4A2. In NSCLC clinical samples, circPTP4A2 expression showed a negative correlation with miR-183-5p levels. Moreover, we demonstrated that circPTP4A2 enhances the expression of EEF2, a downstream target of miR-183-5p. Collectively, our findings elucidate that circPTP4A2 promotes NSCLC progression by sponging miR-183-5p to upregulate EEF2, suggesting it could be a promising therapeutic target for NSCLC.</p>

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CircPTP4A2 (hsa_circ_0007364) promotes growth and invasion of non-small cell lung cancer by regulating miR-183-5p/EEF2 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月8日

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  • Qiuping Shen,
  • Hao Jin,
  • Xiaofeng Zhu

摘要

Recently, a novel circular RNA (circRNA), circPTP4A2 (hsa_circ_0007364), was reported to promote cervical cancer progression. However, its specific role in non-small cell lung cancer (NSCLC) remains unclear. Here, we observed that circPTP4A2 is significantly upregulated in NSCLC tissues and cell lines. Furthermore, multivariate Cox proportional hazards regression analysis confirmed that high circPTP4A2 expression is independently associated with poor prognosis in NSCLC patients after adjusting for confounding clinicopathological covariates. Knockdown of circPTP4A2 significantly suppressed the proliferation, migration, and invasion capabilities of H1299 and A549 cells. Additionally, we identified miR-183-5p as a direct targeted of circPTP4A2. In NSCLC clinical samples, circPTP4A2 expression showed a negative correlation with miR-183-5p levels. Moreover, we demonstrated that circPTP4A2 enhances the expression of EEF2, a downstream target of miR-183-5p. Collectively, our findings elucidate that circPTP4A2 promotes NSCLC progression by sponging miR-183-5p to upregulate EEF2, suggesting it could be a promising therapeutic target for NSCLC.