<p><em>AURKB</em> Promotes the Metastasis of Gastric Cancer, Possibly by Inducing EMT</p>

Abstract

Aim To investigate the function of Aurora kinase B (AURKB) in gastric cancer (GC). Methods Immunohistochemistry was used to assay the expression of AURKB in 50 pairs of GC and adjacent tissues, and qRT-PCR was conducted to test AURKB expression in normal gastric epithelial and GC cell lines. Two segments of small interference RNAs (siRNAs) targeting AURKB were synthesized and inserted into GV248 lentivirus vector. After transfected with LV-AURKB-RNAis, CCK8, wound healing, transwell and flow cytometric assays were performed to determine the influence of silencing AURKB on cell proliferation, invasion, migration, cell cycles and apoptosis of GC cells, and the expression of EMT (epithelial–mesenchymal transition)-related markers was demonstrated by Western blots (WB). Results AURKB was highly expressed in GC and closely associated with lymph node metastasis and advanced stages of GC. Down-regulating AURKB suppressed the proliferation and promoted the apoptosis of GC cells, arrested the cell cycle in G2/M phase, and inhibited the invasion and migration of GC cells. The expression levels of AKT1, mTOR, Myc, MMP2, and VEGFA were decreased, while the expression levels of OCLN and JUP were increased after knocking down of AURKB in both AGC and MKN45 cells. Conclusion AURKB is overexpressed in GC and closely associated with clinicopathologic characteristics of GC. It is likely that by inhibiting VEGFA/Akt/mTOR and Wnt/β-catenin/Myc pathways, silenced AURKB could inhibit the invasive and migratory abilities of GC cells. However, because of the small sample size and the absence of in-vivo experiments, these results should be verified by further studies.

Comprehensive analysis of aberrant alternative splicing related to carcinogenesis and prognosis of papillary thyroid cancer

“…UBE2C and AURKB were recognized as hub genes. Notably, they both play crucial parts in tumor development, metastasis, and drug resistance [ 37 – 41 ]. For example, UBE2C can be increased by estrogen and accelerates epithelial-mesenchymal transition through p53 in endometrial cancer [ 41 ].…”

Cell Cycle Regulation and DNA Damage Response Networks in Diffuse-and Intestinal-Type Gastric Cancer

“…MYC-targeting siRNA, a biologic drug targeting MYC, has been identified to have direct relationship in "Cell cycle: G1/S checkpoint regulation". It has been shown before that the silencing of Aurora kinase B, which is up-regulated in GC, decreased the expression of MYC, arrested the cell cycle in G2/M phase, and inhibited migration of GC [20]. The MYC-targeting siRNA might also be involved in the regulation of cell cycle and EMT.…”

An integrated analysis of prognostic and immune infiltrates for hub genes as potential survival indicators in patients with lung adenocarcinoma

“…Furthermore, AURKB was overexpressed in gastric cancer and was strongly linked to clinicopathological features of the disease. Silencing of AURKB may decrease the invasive and migratory capacities of gastric cancer cells by disrupting the VEGFA/Akt/mTOR and Wnt/-catenin/Myc pathways [ 23 ]. Additionally, AURKB activation was associated with acquired resistance to EGFR TKIs, suggesting that AURKB should be targeted in NSCLC patients scheduled for anti-EGFR treatment but who lack resistance mutations [ 24 ].…”