LAUSR.org creates dashboard-style pages of related content for over 1.5 million academic articles. Sign Up to like articles & get recommendations!

The overexpression of Rab9 promotes tumor progression regulated by XBP1 in breast cancer

Photo from wikipedia

Background Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs). Materials and methods To… Click to show full abstract

Background Rab9 is a small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes and is involved in the recycling of mannose-6-phosphate receptors (MPRs). Materials and methods To determine new treatment strategies for breast cancer and to elucidate the mechanism underlying the phenomenon, we investigated the effects of Rab9 in the human breast cancer cell lines MCF7 and MDA-MB-231. Results We observed that knockdown of Rab9 inhibited the survival and proliferation of MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell survival and proliferation by inducing or suppressing apoptosis. These results were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231 cells, which demonstrated whether the mitochondrial apoptotic pathway was triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and survival and Rab9 changed the expression and phosphorylation of PI3K signaling pathway members. XBP1 is a key regulator of Rab9 and further confirmed that Rab9 play important roles in breast cancer tumorigenesis. Conclusion These data suggest that Rab9 is a good candidate for a novel therapeutic strategy for the treatment of breast cancer.

Keywords: overexpression; cancer; breast cancer; rab9; mcf7 mda

Journal Title: OncoTargets and therapy
Year Published: 2019

Link to full text (if available)


Share on Social Media:                               Sign Up to like & get
recommendations!

Related content

More Information              News              Social Media              Video              Recommended



                Click one of the above tabs to view related content.