HOXB7 induces STAT3‐mediated transformation and lung metastasis in immortalized mammary gland NMuMG cells

Author:

Azuma Kazushi1,Sakamoto Mai12,Katayama Shota1,Matsui Atsuka1,Nakamichi Kazuya1,Goshima Naoki345,Watanabe Shinya6,Nakayama Jun127ORCID,Semba Kentaro16

Affiliation:

1. Department of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan

2. Computational Bio‐Big Data Open Innovation Lab (CBBD‐OIL) National Institute of Advanced Industrial Science and Technology (AIST) Tokyo Japan

3. Division of Transcriptome Analysis, Translational Research Center Fukushima Medical University Fukushima Japan

4. Functional Proteomics Team, Molecular Profiling Research Center for Drug Discovery (molprof) National Institute of Advanced Industrial Science and Technology (AIST) Tokyo Japan

5. Department of Human Sciences Musashino University Tokyo Japan

6. Translational Research Center Fukushima Medical University Fukushima Japan

7. Laboratory of Integrative Oncology National Cancer Center Research Institute Tokyo Japan

Abstract

AbstractThe homeobox family genes are often dysregulated in various cancer types. Particularly HOXB7 amplification and overexpression correlate with poor prognosis in various cancer such as gastric, pancreatic, and lung cancers. Moreover, HOXB7 is known to contribute to cancer progression by promoting epithelial to mesenchymal transition, anticancer drug resistance, and angiogenesis. In this study, we show that HOXB7 is coamplified with ERBB2 in a subset of breast cancer patients and HOXB7 expression correlates with poor prognosis in HER2‐positive breast cancer patients. This clinical observation is supported by the following results—HOXB7 overexpression in an immortalized murine mammary gland epithelial cell line NMuMG induces cellular transformation in vitro, tumorigenesis, and lung metastasis through the activation of JAK‐STAT signaling.

Funder

Japan Society for the Promotion of Science

Publisher

Wiley

Subject

Cell Biology,Genetics

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3