Published online Nov 15, 2022. doi: 10.4251/wjgo.v14.i11.2170
Peer-review started: July 15, 2022
First decision: August 8, 2022
Revised: September 5, 2022
Accepted: October 12, 2022
Article in press: October 12, 2022
Published online: November 15, 2022
Processing time: 123 Days and 0.6 Hours
Gastric cancer (GC) is a common type of digestive cancer with high morbidity and mortality rates worldwide. Considerable effort has been expended in under
To explore the expression and function of miR-30e-3p in GC development.
MiR-30e-3p was found to be downregulated in GC, with low levels thereof predicting poor outcomes among patients with GC. Functionally, we revealed that miR-30e-3p suppressed cell growth and metastatic behaviors of GC cells. Bioinformatics analysis predicted that THO complex 2 (THOC2) was a direct target of miR-30e-3p, and the interaction between miR-30e-3p and THOC2 was further validated by a luciferase reporter assay.
Our findings revealed that knockdown of THOC2 inhibited the growth and metastatic behaviors of GC cells. After investigating signaling pathways involved in miR-30e-3p regulation, we found that the miR-30e-3p/THOC2 axis regulated the PI3K/AKT/mTOR pathway in GC.
Our findings suggest the novel functional axis miR-30e-3p/THOC2 is involved in GC development and progression. The miR-30e-3p/THOC2 axis could be utilized to develop new therapies against GC.
Core Tip: Gastric cancer (GC) is a common digestive cancer with high morbidity and mortality rates worldwide. Considerable effort has been expended in understanding the mechanism of GC development and metastasis. Given that microRNAs have been found to participate in the regulation of GC progression, we explored the expression and function of miR-30e-3p in GC development and revealed that knockdown of THO complex 2 (THOC2) inhibited the growth and metastatic behaviors of GC cells. After investigating signaling pathways involved in miR-30e-3p regulation were investigated, we found that the miR-30e-3p/THOC2 axis regulated the PI3K/AKT/mTOR pathway in GC.