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PMID: 16489016 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer.

Cancer research ·Vol. 66 ·No. 4 ·2006-02-15 ·Pages 2153-61

Kim IM, Ackerson T, Ramakrishna S, Tretiakova M, Wang IC, Kalin TV, Major ML, Gusarova GA, Yoder HM, Costa RH, Kalinichenko VV

Abstract

The proliferation-specific Forkhead Box m1 (Foxm1 or Foxm1b) transcription factor (previously called HFH-11B, Trident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA replication and mitosis. Expression of Foxm1 is found in a variety of distinct human cancers including hepatocellular carcinomas, intrahepatic cholangiocarcinomas, basal cell carcinomas, ductal breast carcinomas, and anaplastic astrocytomas and glioblastomas. In this study, we show that human Foxm1 protein is abundantly expressed in highly proliferative human non-small cell lung cancers (NSCLC) as well as in mouse lung tumors induced by urethane. To determine the role of Foxm1 during the development of mouse lung tumors, we used IFN-inducible Mx-Cre recombinase transgene to delete mouse Foxm1 fl/fl-targeted allele before inducing lung tumors with urethane. We show that Mx-Cre Foxm1-/- mice exhibit diminished proliferation of lung tumor cells causing a significant reduction in number and size of lung adenomas. Transient transfection experiments with A549 lung adenocarcinoma cells show that depletion of Foxm1 levels by short interfering RNA caused diminished DNA replication and mitosis and reduced anchorage-independent growth of cell colonies on soft agar. Foxm1-depleted A549 cells exhibit reduced expression of cell cycle-promoting cyclin A2 and cyclin B1 genes. These data show that Foxm1 stimulates the proliferation of tumor cells during progression of NSCLC.

MeSH Terms
Adenocarcinoma/chemically induced,genetics,metabolism Alleles Animals Carcinoma, Non-Small-Cell Lung/chemically induced,genetics,metabolism,pathology Cell Adhesion Cell Growth Processes/physiology Cyclin A/biosynthesis,genetics Cyclin A2 Cyclin B/biosynthesis,genetics Cyclin B1 DNA Replication DNA, Neoplasm/biosynthesis Forkhead Box Protein M1 Forkhead Transcription Factors/biosynthesis,deficiency,genetics,physiology Gene Deletion Humans Lung Neoplasms/chemically induced,genetics,metabolism,pathology Mice Mice, Inbred C57BL Mice, Transgenic Mitosis RNA, Small Interfering/genetics Urethane
Chemicals
CCNA2 protein, human CCNB1 protein, human Ccnb1 protein, mouse Cyclin A Cyclin A2 Cyclin B Cyclin B1 DNA, Neoplasm FOXM1 protein, human Forkhead Box Protein M1 Forkhead Transcription Factors Foxm1 protein, mouse RNA, Small Interfering Urethane
Authors & Affiliations
11 authors, click to expand affiliations / ORCID
Kim Il-Man
Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Ackerson Timothy
Ramakrishna Sneha
Tretiakova Maria
Wang I-Ching
Kalin Tanya V
Major Michael L
Gusarova Galina A
Yoder Helena M
Costa Robert H
Kalinichenko Vladimir V
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
2006-02-15
Pages
2153-61
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
Grants
NIDDK NIH HHS · DK 54687-06 · United States
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