Esophageal squamous cell carcinoma (ESCC) is recognized as one of the malignant tumors with poor prognosis. UAP1L1 (UDP‐N‐acetylglucosamine‐1‐like‐1) affects numerous biological processes, which is a key regulator of the development of malignant tumors. The biological function and molecular mechanism of UAP1L1 in ESCC were explored in this study. The relationship between UAP1L1 and ESCC was analyzed by immunohistochemical staining, revealing the high expression of UAP1L1 in ESCC. Importantly, the increased expression of UAP1L1 indicated the deterioration of patients’ condition, which has clinical significance. Furthermore, the loss‐of‐function assays demonstrated that knockdown of UAP1L1 inhibited the progression of ESCC on suppressing proliferation, hindering migration, and enhancing apoptosis in vitro. Moreover, the apoptosis of ESCC cells was induced by knockdown of UAP1L1 via regulating a variety of apoptosis‐related proteins, such as upregulation of Bax, CD40, CD40L, Fas, FasL, IGFBP‐6, p21, p27, p53, and SMAC. Additionally, further investigation indicated that UAP1L1 by affecting the PI3K/Akt, CCND1, and MAPK promotes the progression of ESCC. In vivo xenograft model further confirmed that knockdown of UAP1L1 inhibited the development of ESCC. In conclusion, UAP1L1 was involved in the development and progression of ESCC, which may provide a powerful target for future molecular therapies.

中文翻译：

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沉默UAP1L1可抑制食管鳞癌的增殖并诱导其凋亡

食管鳞状细胞癌（ESCC）被认为是预后较差的恶性肿瘤之一。UAP1L1（UDP‐ N-乙酰氨基葡萄糖-1-类）影响许多生物学过程，这是恶性肿瘤发展的关键调节器。本研究探讨了UAP1L1在ESCC中的生物学功能和分子机制。通过免疫组织化学染色分析了UAP1L1与ESCC之间的关系，揭示了UAP1L1在ESCC中的高表达。重要的是，UAP1L1表达的增加表明患者病情恶化，具有临床意义。此外，功能丧失试验证明，敲除UAP1L1可以抑制ESCC的进展，从而抑制了增殖，阻碍了迁移并增强了体外的细胞凋亡。此外，通过调节多种凋亡相关蛋白（如上调Bax，CD40，CD40L，Fas，FasL，IGFBP-6，p21，p27，p53和SMAC。此外，进一步的研究表明，UAP1L1通过影响PI3K / Akt，CCND1和MAPK促进了ESCC的发展。体内异种移植模型进一步证实，敲除UAP1L1可抑制ESCC的发展。总之，UAP1L1参与了ESCC的发展和进程，这可能为将来的分子疗法提供有力的靶标。