胆管癌（CCA）以其侵袭性而闻名，在当前的医学领域，特别是在靶向治疗方面，提出了巨大的挑战。在此背景下，长链非编码RNA（lncRNA）引起了研究人员的关注。这些独特的RNA被认为在各种癌症中发挥着关键作用，为开发更有效的治疗策略提供了有希望的途径。先前的研究已经证实了 APCDD1L-DT 在许多人类肿瘤中的异常表达，证明了其在疾病进展中的积极调节作用。然而，APCDD1L-DT 在 CCA 中的生物学功能仍不完全清楚。这项研究标志着 APCDD1L-DT 在 CCA 标本中表现出异常表达的首次记录，与肿瘤患者的 TNM 分期建立了密切的相关性。此外，抑制 APCDD1L-DT 表达会阻碍肿瘤细胞的活力和运动性。从机制上讲，转录因子 ZNF460 的异常激活正向调节 CCA 中 APCDD1L-DT 的表达。这种激活反过来又促进 Wnt 通路的异常激活，通过阻止泛素介导的 DVL2 降解来促进肿瘤的发展。从广义上讲，这项研究为理解 CCA 提供了有利的视角，并为解决这种令人畏惧的恶性肿瘤提供了支持。© 2024。作者获得 Springer Nature America, Inc. 的独家许可。

Cholangiocarcinoma (CCA), known for its aggressive nature, poses a formidable challenge in the current medical landscape, particularly in targeted therapies. Against this backdrop, long non-coding RNAs (lncRNAs) have captured the attention of researchers. These unique RNAs are believed to play pivotal roles in various cancers, offering promising avenues for the development of more effective treatment strategies. Previous studies have substantiated the aberrant expression of the APCDD1L-DT in numerous human tumors, demonstrating its positive regulatory roles in disease progression. Nevertheless, the biological functions of APCDD1L-DT in CCA are still not fully understood. This study marks the inaugural documentation of APCDD1L-DT exhibiting aberrant expression in CCA specimen, establishing a close correlation with the TNM staging of tumor patients. Furthermore, suppressing APCDD1L-DT expression hinders both the viability and motility of tumor cells. Mechanistically, the abnormal activation of the transcription factor ZNF460 positively regulated APCDD1L-DT expression in CCA. This activation, in turn, propels the abnormal activation of the Wnt pathway, fostering tumor development by impeding the ubiquitin-mediated degradation of DVL2. Broadly speaking, this study provides auspicious perspectives for comprehending CCA and furnishes support for addressing this daunting malignancy.© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.