Show simple item record

dc.contributor.authorLi, Ling
dc.contributor.authorTang, Wenhua
dc.contributor.authorWu, Xiaoqing
dc.contributor.authorKarnak, David
dc.contributor.authorMeng, Xiaojie
dc.contributor.authorThompson, Rachel
dc.contributor.authorHao, Xinbao
dc.contributor.authorLi, Yongmin
dc.contributor.authorQiao, Xiaotan T.
dc.contributor.authorLin, Jiayuh
dc.contributor.authorFuchs, James R.
dc.contributor.authorSimeone, Diane M.
dc.contributor.authorChen, Zhi-Nan
dc.contributor.authorLawrence, Theodore S.
dc.contributor.authorXu, Liang
dc.identifier.citationLi, L., W. Tang, X. Wu, D. Karnak, X. Meng, R. Thompson, X. Hao, Y. Li, X. T. Qiao, J. Lin, J. Fuchs, D. M. Simeone, Z.-N. Chen, T. S. Lawrence, and L. Xu. "HAb18G/CD147 Promotes PSTAT3-Mediated Pancreatic Cancer Development via CD44s." Clinical Cancer Research 19.24 (2013): 6703-715.en_US

STAT3 plays a critical role in initiation and progression of pancreatic cancer. However, therapeutically targeting STAT3 is failure in clinic. We previously identified HAb18G/CD147 as an effective target for cancer treatment. In this study, we aimed to investigate potential role of HAb18G/CD147 in STAT3-involved pancreatic tumorigenesis in vitro and in vivo.

Experimental Design

The expression of HAb18G/CD147, pSTAT3 and CD44s were determined in tissue microarrays. The tumorigenic function and molecular signaling mechanism of HAb18G/CD147 was assessed by in vitro cellular and clonogenic growth, reporter assay, immunoblot, immunofluorescence staining, immunoprecipitation, and in vivo tumor formationusing loss or gain-of-function strategies.


Highly expressed HAb18G/CD147 promoted cellular and clonogenic growth in vitro and tumorigenicity in vivo. CyPA, a ligand of CD147, stimulated STAT3 phosphorylation and its downstream genes cyclin D1/survivin through HAb18G/CD147 dependent mechanisms. HAb18G/CD147 was associated and co-localized with cancer stem cell marker CD44s in lipid rafts. The inhibitors of STAT3 and survivin, as well as CD44s neutralizing antibodies suppressed the HAb18G/CD147-induced cell growth. High HAb18G/CD147 expression in pancreatic cancer was significantly correlated with the poor tumor differentiation, and the high co-expression of HAb18G/CD147-CD44s-STAT3 associated with poor survival of patients with pancreatic cancer.


We identified HAb18G/CD147 as a novel upstream activator of STAT3 via interacts with CD44s and plays a critical role in the development of pancreatic cancer. The data suggest HAb18G/CD147 could be a promising therapeutic target for highly aggressive pancreatic cancer and a surrogate marker in the STAT3-targeted molecular therapies.
dc.publisherAmerican Association for Cancer Researchen_US
dc.subjectPancreatic canceren_US
dc.subjectTumor developmenten_US
dc.titleHAb18G/CD147 Promotes pSTAT3-Mediated Pancreatic Cancer Development via CD44sen_US
kusw.kuauthorWu, Xiaoqing
kusw.kudepartmentHiguchi Biosciences Centeren_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US

Files in this item


This item appears in the following Collection(s)

Show simple item record