Overexpressed PKMYT1 promotes tumor progression and associates with poor survival in esophageal squamous cell carcinoma

过度表达的 PKMYT1 促进肿瘤进展并与食管鳞状细胞癌的低生存率相关

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作者:Qingyi Zhang #, Xuan Zhao #, Chaoqi Zhang, Wei Wang, Feng Li, Donglei Liu, Kai Wu, Dengyan Zhu, Shasha Liu, Chunyi Shen, Xin Yuan, Kai Zhang, Yang Yang, Yi Zhang, Song Zhao

Background

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors worldwide and the 5-year overall survival rate remains poor. Protein kinase, membrane associated tyrosine/threonine (PKMYT1) is overexpressed in several cancers and participate in tumor progression. However, the mechanism of PKMYT1 in ESCC is unclear.

Conclusion

PKMYT1 plays an crutial role in ESCC progression, downregulated PKMYT1 might inhibit the development of ESCC by AKT/mTOR signaling pathway, and might be a novel target in the treatment of ESCC.

Methods

We detected the expression of PKMYT1 in ESCC patients and analysed the correlation with overall survival time and disease-free survival time. Then we detected PKMYT1 expression in ESCC cell lines and immortalized human esophageal epithelial cell line. Down-regulated PKMYT1 was carried out in KYSE70 and KYSE450 cells to invetigate the mechanism of PKMYT1 in ESCC cells.

Purpose

The objective of our study was to demonstrate the the expression and role of PKMYT1 in ESCC. Patients and

Results

PKMYT1 was up-regulated in tumor tissues and ESCC cell lines, and higher expression of PKMYT1 correlated with poorer overall survival in ESCC patients. Besides, in ESCC cell lines KYSE70 and KYSE450, knocking down PKMYT1 allowed more cells to skip G2/M checkpoint to complete mitosis, which promoted cell apoptosis, inhibited cell proliferation, and prevented the EMT phenotype in vitro. Meantime, we also observed that down-regulated PKMYT1 in ESCC cells suppressed AKT/mTOR signaling pathway. These results demonstrated PKMYT1 may act as an oncogene in ESCC.

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