FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma

Lisha Qi; Wangzhao Song; Lingmei Li; Lu Cao; Yue Yu; Chunmin Song; Yalei Wang; Fei Zhang; Yang Li; Bin Zhang; Wenfeng Cao

doi:10.18632/oncotarget.12187

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma

Lisha Qi, Wangzhao Song, Lingmei Li, Lu Cao, Yue Yu, Chunmin Song, Yalei Wang, Fei Zhang, Yang Li, Bin Zhang _ and Wenfeng Cao

PDF | HTML | Supplementary Files | How to cite

Oncotarget. 2016; 7:74015-74030. https://doi.org/10.18632/oncotarget.12187

Metrics: PDF 2443 views | HTML 3872 views | ?

Abstract

Lisha Qi1,5,6, Wangzhao Song1,4,5,6, Lingmei Li1,5,6, Lu Cao1,4,5,6, Yue Yu2,5,6, Chunmin Song8, Yalei Wang1,5,6, Fei Zhang5,6,7, Yang Li3,4,5,6, Bin Zhang2,5,6, Wenfeng Cao1,5,6

1Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China

2Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China

3Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China

4Tianjin Medical University, Tianjin 300070, China

5The Key Laboratory of Tianjin Cancer Prevention and Treatment, Tianjin 300060, China

6National Clinical Research Center for Cancer, Tianjin 300060, China

7Research Center of Basic Medical Sciences, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China

8Department of Family Planning, Maternity & Child Care Center of Luoyang, Luoyang 471000, China

Correspondence to:

Bin Zhang, email: [email protected]

Wenfeng Cao, email: [email protected]

Keywords: FGF4, epithelial-mesenchymal transition, store-operated calcium entry, Orai1, FGF7

Received: February 04, 2016 Accepted: August 23, 2016 Published: September 22, 2016

ABSTRACT

Several fibroblast growth factor (FGF) isoforms act to stimulate epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7 are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC) cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell morphology, promoted EMT-associated protein expression, and enhanced cell proliferation, migration/invasion and colony initiation. In addition, FGF4 increased store-operated calcium entry (SOCE) and expression of the calcium signal-associated protein Orai1. The SOCE inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or Orai1 knockdown reversed all of the EMT-promoting effects of FGF4. BHQ also inhibited FGF4-induced EMT in a mouse xenograft model. Finally, 60 human lung ADC samples and 21 sets of matched specimens (primary and metastatic foci in lymph nodes from one patient) were used to confirm the clinicopathologic significance of FGF4 and its correlation with E-cadherin, Vimentin and Orai1 expression. Our study thus shows that FGF4 induces EMT by elevating SOCE in lung ADC.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 12187

Publication Alerts

Research Papers:

FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma

Abstract