MiR-4429 prevented gastric cancer progression through targeting METTL3 to inhibit m6 A-caused stabilization of SEC62
Abstract
Gastric cancer (GC) has been recognized as the major reason for global cancer-associated mortality. SEC62 homolog, preprotein translocation factor (SEC62) has been documented to possess carcinogenic functions in cancers, but its influence on GC remains elusive. Present study aimed to uncover the impact and mechanism of SEC62 in GC. We validated the upregulation of SEC62 in GC samples by GEPIA, and revealed its high level in GC cell lines. Functionally, depletion of SEC62 hindered proliferation and encouraged apoptosis in GC cells. Furthermore, we found through Starbase 3.0 and validated that methyltransferase like 3 (METTL3) interacted with SEC62 to induce the m6A on SEC62 mRNA, therefore facilitated the stabilizing effect of IGF2 binding protein 1 (IGF2BP1) on SEC62 mRNA. Moreover, we predicted through miRmap and validated that miR-4429 targeted and inhibited METTL3 to repress SEC62. Rescue assays demonstrated that miR-4429 inhibited GC progression through METTL3/SEC62 axis. Together, our study firstly revealed that miR-4429 prevented gastric cancer progression through targeting METTL3 to inhibit m6A-caused stabilization of SEC62, indicating miR-4429 as a promising target for treatment improvement for GC.
References
Citations
Related Concepts
Related Feeds
Apoptosis in Cancer
Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.
Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis