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MED28 modulates transcription factor FOXM1‐associated migration and invasion in human non‐small cell lung cancer (NSCLC) cells
Author(s) -
Hsieh NienTsu,
Huang ChunYin,
Li ChienCheng,
Wang IChing,
Lee MingFen
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.668.4
Subject(s) - foxm1 , carcinogenesis , cancer research , biology , transcription factor , lung cancer , metastasis , matrigel , non small cell lung cancer (nsclc) , small hairpin rna , cancer , cell , microbiology and biotechnology , medicine , oncology , gene knockdown , cell culture , gene , a549 cell , genetics , angiogenesis
Lung cancer has become a leading cause of cancer deaths worldwide, where non‐small cell lung cancer (NSCLC) accounts for the majority of the diagnosed cases. Increased expression of transcription factor Forkhead Box M1 (FOXM1) is involved in the unfavorable development of several types of cancer, including lung tumor aggressiveness. MED28 exhibits multiple cellular roles, including a Mediator subunit for transcription, an interactor with merlin, Src kinases, Grb2 and cytoskeleton‐associated proteins, which is involved in many cellular signaling pathways. Our laboratory has previously found that MED28 appears to modulate the development of epithelial‐mesenchymal transition and invasion in human NSCLC cells. The objective of the current study is to investigate the potential role of MED28 in FOXM1‐associated tumorigenesis in NSCLC. MED28 expression positively corresponded to both migration and Matrigel invasion events. Inducible expression of FOXM1 not only enhanced NSCLC cell migration and Matrigel invasion but also significantly inhibited siMED28‐mediated suppression of cell invasiveness. Suppression of MED28 reduced the expression of FOXM1 as well as MMP2, a metastasis marker and downstream target of FOXM1. MED28 also regulated the luciferase activity of the MMP2‐reporter gene. Taken together, our data indicate an important connection between MED28 and FOXM1 in the progression of malignancy in NSCLC. Support or Funding Information This work was supported by the grants NSC102‐2320‐B‐309‐001‐MY3 and MOST106‐2320‐B‐309‐001‐MY3 to M‐F Lee. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .