KIAA1199 promotes migration and invasion by Wnt/β-catenin pathway and MMPs mediated EMT progression and serves as a poor prognosis marker in gastric cancer

Abstract

BackgroundKIAA1199 was upregulated in diverse cancers, but the association of KIAA1199 with gastric cancer (GC), the biological role of KIAA1199 in GC cells and the related molecular mechanisms remain to be elucidated.MethodsKIAA1199 expression was analysed by reverse transcription-polymerase chain reaction assay (RT-PCR) and immunohistochemistry (IHC) in GC patient tissue. The small hairpin RNA (shRNA) was applied for the knockdown of endogenous KIAA1199 in NCI-N87 and AGS cells. MTT, colony formation, scratch wounding migration, transwell chamber migration and invasion assays were employed respectively to investigate the role of KIAA1199 in GC cells. The potential signaling pathway of KIAA1199 induced migration and invasion was detected.ResultsKIAA1199 was upregulated in GC tissue and was an essential independent marker for poor prognosis. Knockdown KIAA1199 suppressed the proliferation, migration and invasion in GC cells. KIAA1199 stimulated the Wnt/β-catenin signaling pathway and the enzymatic activity of matrix metalloproteinase (MMP) family members and thus accelerated the epithelial-to-mesenchymal transition (EMT) progression in GC cells.ConclusionThese findings demonstrated that KIAA1199 was upregulated in GC tissue and associated with worse clinical outcomes in GC, and KIAA1199 acted as an oncogene by promoting migration and invasion through the enhancement of Wnt/β-catenin signaling pathway and MMPs mediated EMT progression in GC cells.

Nicotinamide N-methyltransferase promotes epithelial-mesenchymal transition in gastric cancer cells by activating transforming growth factor-β1 expression

“…In China, the incidence of gastric cancer is the second highest of all the malignant tumors (1,2). Early symptoms in the majority of patients with gastric cancer are not detected (3). The prognosis remains poor in patients with intermediate-and advanced-stage gastric cancer and the total 5-year survival rate is ~20% (3).…”

Induction of CEMIP in Chondrocytes by Inflammatory Cytokines: Underlying Mechanisms and Potential Involvement in Osteoarthritis

“…Upregulation of CEMIP has also been reported in multiple solid tumors, and it is recognized as an oncogenic protein. Moreover, CEMIP was reported to play a role in epithelial-to-mesenchymal transition (EMT) through Wnt/β-catenin signaling [16]. Values represent mean ± SD (a, mRNA, n = 6 per group; b, protein, n = 3 per group).…”

“…Upregulation of CEMIP has also been reported in multiple solid tumors, and it is recognized as an oncogenic protein. Moreover, CEMIP was reported to play a role in epithelial-to-mesenchymal transition (EMT) through Wnt/β-catenin signaling [16]. Yoshida et al were the first to report a relationship between CEMIP and OA by showing that CEMIP is involved in HA catabolism [17].…”

Hepatitis B virus x protein induces epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating long non-coding RNA

“…Of them, the Wnt pathway is a well-known pathway associated with EMT, and the components of this pathway are involved in the EMT process [ 33 , 34 ]. For example, β-catenin can translocate from the cytoplasm to the nucleus, where it regulates the expression of some genes associated with migration and invasion [ 35 ]. The activation of Wnt signalling can also up-regulate EMT-associated regulators, such as Snail and ZEB1 [ 36 , 37 ].…”