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EPS8L3 suppresses apoptosis and autophagy of gastric cancer through PI3K/AKT/mTOR signaling

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Abstract

Backgrounds

Epidermal growth factor receptor kinase substrate 8-like 3 (EPS8L3) functions as a substrate of EGFR, and regulates signalings involved in cell proliferation, differentiation, and migration. The oncogenic role of EPS8L3 in distinct tumors was widely investigated, while the effect of EPS8L3 on gastric cancer (GC) remains unknown.

Objectives

To investigate the effect of EPS8L3 on gastric cancer (GC).

Results

EPS8L3 was elevated in GC tissues and cells, and predicted poor prognosis in the patients. Over-expression of EPS8L3 increased cell viability and reduced apoptosis of GC. However, cell viability of GC was decreased and the apoptosis was promoted by silence of EPS8L3. Knockdown of EPS8L3 down-regulated protein expression of p62, while up-regulated Beclin1 and LC3-II/LC3-I in GC cells. Phosphorylation of PI3K, AKT, and mTOR in GC cells was inhibited by EPS8L3 silence.

Conclusion

EPS8L3 functioned as an oncogene in GC through suppression of cell apoptosis and autophagy via activation of PI3K/AKT/mTOR signaling.

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Authors

Contributions

LY designed the study and carried them out. LX supervised the data collection, analyzed the data, and interpreted the data. SJ prepared the manuscript for publication and reviewed the draft of the manuscript. All authors have read and approved the manuscript.

Corresponding author

Correspondence to Shuxuan Jin.

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Conflict of interests

The authors state that there are no conflicts of interest to disclose. Licai You declares that he/she has no conflict of interest; Lijing Xiao declares that he/she has no conflict of interest; Shuxuan Jin declares that he/she has no conflict of interest.

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This article does not contain any studies with human participants or animals performed by any of the authors.

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You, L., Xiao, L. & Jin, S. EPS8L3 suppresses apoptosis and autophagy of gastric cancer through PI3K/AKT/mTOR signaling. Mol. Cell. Toxicol. 19, 373–381 (2023). https://doi.org/10.1007/s13273-022-00266-6

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  • DOI: https://doi.org/10.1007/s13273-022-00266-6

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