Esophageal cancer (ESCA) is a global dead malignancy with poor prognosis. However, its underlying molecular mechanism remains to be elucidated. Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) has been reported as a tumor suppressor in multisystem cancer but its function in ESCA has not been reported. We analyzed LHPP expression between normal and tumor tissues of ESCA patients and performed LHPP overexpression on the ESCA cells KYSE-150 (K150). We did not observe significant differences in the expression level of LHPP between ESCA and normal tissue, and noticed that LHPP expression was not related to ESCA patient survival rate. However, increased expression of LHPP in K150 cells induced mitochondrial dysfunction, inhibited cell proliferation, migration, and cell cycle, and simultaneously increased cell apoptosis. Besides, we found that K150 cells underwent mitotic catastrophe after overexpressing LHPP, which may be regulated through the P27/cyclin A/cdk2 signaling pathway. Although the expression of LHPP may not be related to the progression and prognosis of ESCA, mitotic catastrophe, a new mechanism of tumor suppressor function of LHPP was found after overexpressing LHPP in ESCA cells.

Data Availability

The data used to support the findings of this study are included within the article.

中文翻译：

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磷酸赖氨酸磷酸组氨酸无机焦磷酸磷酸酶通过 P27/cyclin A/CDK2 信号通路诱导有丝分裂灾难抑制人食管癌细胞生长

食管癌（ESCA）是一种预后不良的全球性致命恶性肿瘤。然而，其潜在的分子机制仍有待阐明。磷酸赖氨酸磷酸组氨酸无机焦磷酸磷酸酶 (LHPP) 已被报道为多系统癌症的肿瘤抑制因子，但其在 ESCA 中的功能尚未报道。我们分析了 ESCA 患者正常组织和肿瘤组织之间的 LHPP 表达，并在ESCA 细胞KYSE-150 (K150)上进行了 LHPP 过表达。我们没有观察到 ESCA 和正常组织之间 LHPP 表达水平的显着差异，并注意到 LHPP 表达与 ESCA 患者生存率无关。然而，K150细胞中LHPP表达增加会导致线粒体功能障碍，抑制细胞增殖、迁移和细胞周期，同时增加细胞凋亡。此外，我们发现K150细胞在过表达LHPP后经历了有丝分裂灾难，这可能是通过P27/cyclin A/cdk2信号通路来调节的。虽然LHPP的表达可能与ESCA、有丝分裂灾难的进展和预后无关，但在ESCA细胞中过表达LHPP后，发现了LHPP抑癌功能的新机制。

数据可用性

用于支持本研究结果的数据包含在文章中。