Eukaryotic Elongation Factor 1Alpha-2 (EEF1A2) Participates in the Progression of Gastric Cancer via Interaction with Heat Shock Protein B8 (HSPB8)

Objective: The critical roles of eukaryotic elongation factor 1alpha-2 (EEF1A2) and heat shock protein B8 (HSPB8) in the carcinogenesis and progression of cancers have been well documented. However, the regulatory role of EEF1A2/HSPB8 in the development of gastric cancer (GC) have not been fully understood. This study was aimed at clarifying the biological effects of EEF1A2/HSPB8 on the malignant behaviors of GC cells and to investigate the molecular mechanism underlying the involvement of EEF1A2/HSPB8 in GC.

Methods: In the present work, expression differences of EEF1A2 and HSPB8 in GC cells were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot assay. Cell counting kit -8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) staining, wound healing and transwell assays were employed to detect the proliferation, migration and invasion of GC cells. In addition, tube formation assay was adopted to assess in vitro angiogenesis of HUVECs incubated with the conditioned media (CM) of GC cells. Moreover, the interaction between EEF1A2 and HSPB8 was predicted from BioGrid database and analyzed through co-immunoprecipitation (Co-IP).

Results: The present research revealed that EEF1A2 and HSPB8 were highly expressed in GC cell lines. EEF1A2 knockdown markedly suppressed the proliferation, migration and invasion of GC cells as well as in vitro angiogenesis. Furthermore, it was verified that EEF1A2 interacted with HSPB8 and positively regulated HSPB8 expression. Overexpression of HSPB8 reversed the suppressive effects of EEF1A2 knockdown on GC cell proliferation, migration, invasion and in vitro angiogenesis.

Conclusion: In conclusion, EEF1A2 could act as an oncogene in the development of GC via promoting HSPB8 expression.