Abstract
Beta-catenin/TCF signaling has been reported to promote the growth and metastasis of pancreatic cancer cells. However, the regulation for the beta-catenin/TCF transcriptional complex remains largely unknown. Here, we have found that YEATS4 is a positive regulator for Beta-catenin/TCF signaling. The expression of YEATS4 was elevated in clinical pancreatic cancer samples and pancreatic cancer mouse model. Up-regulation of YEATS4 promoted the growth, migration and invasion of pancreatic cancer cells, while knocking down the expression of YEATS4 inhibited the growth, migration, invasion and metastasis of pancreatic cancer cells. Moreover, the mechanism study revealed that YEATS4 interacted with beta-catenin and activated beta-catenin/TCF signaling. Furthermore, knocking down the expression of YEATS4 impaired the malignant transformation of normal pancreatic cells (HPDE6C7) by the oncogenic Ras. Taken together, our study demonstrated the oncogenic roles of YEATS4 in the progression of pancreatic cancer by activating beta-catenin/TCF signaling and suggested that YEATS4 might be a promising therapeutic target for pancreatic cancer.
Highlights
Numerous studies have demonstrated the roles of Wnt/ beta-catenin signaling in cell proliferation, differentiation and motility [1]
We have demonstrated that YEATS4 promoted the growth, migration and invasion of pancreatic www.impactjournals.com/oncotarget cancer cells by activating beta-catenin/TCF signaling
The expression of YEATS4 was increased in the clinical pancreatic cancer samples, which was confirmed by the oncomine database and our experimental results, suggesting that YEATS4 might be diagnosis marker for Pancreatic ductal adenocarcinoma (PDAC)
Summary
Numerous studies have demonstrated the roles of Wnt/ beta-catenin signaling in cell proliferation, differentiation and motility [1]. Beta-catenin is the key molecule in the Wnt/ beta-catenin pathway [2]. The protein level of beta-catenin is tightly controlled by the destruction complex which contained APC, Axin and GSK3beta. The stimulation of Wnt ligand releases beta-catenin from the destruction complex, which leads to the cytoplasmic accumulation and nuclear localization of beta-catenin. Beta-catenin formes a complex with TCF4 (T-cell factor 4) and promotes the transcription of multiple genes [3]. The regulation for beta-catenin/TCF complex remains largely unknown
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