Background
Gastric cancer (GC) is a highly occurring cancer with poor prognosis. Reports indicate that long non-coding RNA (LncRNA) potentially regulates tumor progression. Herein, we
Conclusion
AC118344.1 promotes gastric cancer cell proliferation and invasion and lung metastasis in nude mice by upregulating the expression of AKT2 and its downstream molecules (HK2 and MMP2). Therefore, our findings provide a novel mechanism of the AC118344.1-AKT2-HK2/MMP2 axis in regulating the development of gastric cancer cells.
Methods
Overexpression and knockout experiments were used to clarify the potential molecular signaling mechanisms induced by AC118344.1. CCK-8, transwell and in vivo metastasis assay were used to detect the function of AC118344.1 in AGS and SGC-7901 cells. Additionally, shRNA silencing techniques, qRT-PCR and Western blot assay were used to explore the relationship between AC118344.1, AKT2, and its downstream molecules.
Results
Upregulating the expression of AC118344.1 induces cell proliferation, invasion in vitro, and lung metastasis in vivo whereas downregulating the expression of AC118344.1 inhibits these effects. Besides, silencing the expression of AC118344.1 downregulated the expression of AKT2 in both the two cells. On the other hand, silencing the expression of AKT2 by shRNA was unable to downregulate the expression of AC118344.1 in both the gastric cancer cells. Also, AC118344.1 regulated AKT2 via its downstream molecules including HK2 and MMP2.