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This review uncovers the interplay of YAP and PCNP in esophageal carcinoma, highlighting tumor growth and therapeutic targets.
Esophageal cancer is one of the malignant tumors with high incidence and mortality rates worldwide. Its occurrence and development involve abnormal regulation of multiple signaling pathways. In recent years, the role of Hippo signaling and PEST-containing nuclear protein (PCNP) in esophageal cancer has gradually received attention. As a key regulator of organ size and tissue homeostasis, the Hippo pathway exerts its biological effects primarily through its core effector Yes-associated protein (YAP)/TAZ; accumulating evidence confirms that aberrant activation of YAP is closely linked to esophageal cancer occurrence, progression, lymph node metastasis, and chemoresistance, making it a critical oncogenic driver. PCNP, a highly conserved nuclear protein, together with its E3 enzyme NIRF, is involved in modulating cell cycle progression, DNA damage repair, and apoptotic signaling under physiological conditions. However, its overexpression in esophageal cancer tissues has been associated with accelerated tumor growth and unfavorable patient outcomes, potentially through interactions with downstream oncogenic mediators such as NRF2. This review summarizes the research progress on the Hippo pathway and PCNP, and proposes a possible mechanistic interplay between them in esophageal cancer based on their functions, focusing on exploring their mechanisms of action, regulatory relationships, and potential therapeutic targets in the occurrence and development of esophageal cancer, in order to provide ideas for diagnosis, prognosis, and targeted therapy of esophageal cancer.
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Sun et al. (2025) studied this question.
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