Fig. 8: Schematic diagram deciphering the mechanisms by which ROBO1, G3BP2 and eIF3A form hetero-complex to mediate radio-resistance in ESCC cells.

Mechanistically, ROBO1 interacted with G3BP2 and eIF3A to form heterocomplex and accelerated eIF3A degradation through activating lysosome signaling pathway in ESCC cells. Under irradiation exposure, free eIF3A inactivated mTOR signaling and downreglated its downstream DNA nucleotide excision repair (NER) genes expression through directly promoting P53 translation, which finally attenuated ESCC radioresistance and retarded cancer severity.