journal contribution
posted on 2023-03-31, 01:00 authored by Fanyang Kong, Xiangyu Kong, Yiqi Du, Ying Chen, Xuan Deng, Jianwei Zhu, Jiawei Du, Lei Li, Zhiliang Jia, Dacheng Xie, Zhaoshen Li, Keping Xie One file contains 3 Supplementary Tables: Supplementary Table S1. Clinicopathologic characteristics of the PDAC patients from whom the TMA specimens were obtained; Supplementary Table S2. STK33 protein expression in PDAC TMA specimens and its relationship with patient clinicopathologic characteristics; Supplementary Table S3. The sequences of the gene-specific primers used in real-time PCR analysis, vector constructs, and ChIP analysis
Funding
National Cancer Institute
Shanghai Yang Fan Project
National Natural Science Foundation of China
History
ARTICLE ABSTRACT
The serine/threonine kinase STK33 has been implicated in cancer cell proliferation. Here, we provide evidence of a critical role for STK33 in the pathogenesis and metastatic progression of pancreatic ductal adenocarcinoma (PDAC). STK33 expression in PDAC was regulated by the hypoxia-inducible transcription factor HIF1α. In human PDAC specimens, STK33 was overexpressed and associated with poor prognosis. Enforced STK33 expression promoted PDAC proliferation, migration, invasion, and tumor growth, whereas STK33 depletion exerted opposing effects. Mechanistic investigations showed that HIF1α regulated STK33 via direct binding to a hypoxia response element in its promoter. In showing that dysregulated HIF1α/STK33 signaling promotes PDAC growth and progression, our results suggest STK33 as a candidate therapeutic target to improve PDAC treatment. Cancer Res; 77(24); 6851–62. ©2017 AACR.
