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00085472can170067-sup-177093_2_supp_4207221_ddh31y.pdf (85.07 kB)

Supplementary Tables from STK33 Promotes Growth and Progression of Pancreatic Cancer as a Critical Downstream Mediator of HIF1α

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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.

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    Cancer Research

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    Keywords

    AngiogenesisAngiogenic factors and receptorsBiomarkersGastrointestinal CancersPancreatic cancerGene RegulationMechanisms of transcription

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