EFL1 (Elongation Factor Like GTPase 1)

Treatment of the MIA PaCa-2 with EFL1 or EFL3 increased the levels of phosphorylated inositol-requiring enzyme 1 alpha (IRE1α), activating transcription factor 4 (ATF4) and CHOP, involved in the endoplasmic reticulum (ER) stress pathway and cleaved poly (ADP-ribose) polymerase protein (PARP), as apoptotic markers, and inhibited cell proliferation. Thus, EFL1 and EFL3 may be useful in the development of treatments for pancreatic cancer.

Overall, our integrated computational and experimental approach provides a comprehensive understanding of how specific mutations in SBDS alter its structural dynamics and binding interactions. These insights enhance our broader understanding of SBDS function and its role in ribosome biogenesis.

Low Eif6 levels reduced Tp53 pathway activation but did not rescue neutropenia in Sbds-deficient zebrafish. Further studies elucidating the interplay between SBDS, EIF6, TP53, and cellular stress responses offer promising insights into SDS pathogenesis, somatic genetic rescue, and therapeutic strategies.

The morphology of the F-actin cytoskeleton was destroyed. These findings indicated that EFL1 caused cytotoxicity in the human intestinal Caco-2 cells through mitochondrial damage, inhibition of the energy metabolism, and suppression of the ion and water molecule transporters, as well as the down-regulation tight junction and cytoskeleton protiens.

Furthermore, overexpression of DDR1 abolished the anti-liver metastasis effect and pro-immune infiltration action of EFL1 in SHI mice. Together, our findings suggested that EFL1 protects against breast cancer liver metastasis in vivo by targeting DDR1-mediated immune infiltration.