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Overexpression of Sp1 transcriptoin factor in tumor cells reduced cell proliferation
Author(s) -
Hung JanJong,
Wu ChienHsing
Publication year - 2008
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.22.1_supplement.838.3
Subject(s) - a549 cell , cell cycle , biology , hela , mitosis , carcinogenesis , cell growth , nocodazole , microbiology and biotechnology , cancer cell , cell , cancer research , cancer , genetics , cytoskeleton
The transcription factor Sp1 is expressed in different cells and thereby regulates the expression of genes involved in many cellular processes including cell cycle regulation, apoptosis, and differentiation. Previous studies have revealed that the expression of Sp1 is maintained in several types of cancer such as gastric cancer. However, the recent studies and our preliminary data revealed that accumulation of Sp1 led to tumor cells death. In our data, we found that more expression of Sp1 in the most cancer tissues was observed compared to the normal tissues, especially lung cancer. In this study, we chose non‐small cell lung cancer (NSCLC): (A549) to character the role of Sp1 during tumorigenesis. At first, adeno‐constructs including adeno‐GFP and adeno‐GFP‐Sp1 have succeeded to be made to infect the HeLa cells completely. We found that Sp1 regulated cell proliferation negatively in A549 cell by counting the cell number and the MTS assay. In the nude mice system, HeLa and A549 cells infected with adeno‐GFP and adeno‐GFP‐Sp1 viruses to overexpress the Sp1, to be injected into the nude mice, the tumors in the mice injected with adeno‐GFP injected cells were larger than those injected with adeno‐GFP‐Sp1 injected cells. Both of sub‐G1 and cell cycle arrest were observed in adeno‐GFP‐Sp1 injected cells by FACS analysis. Furthermore, we also used the Nocodazole and thymidine to synchronize cells in Mitosis and G1 phase respectively to study the role of overexpressed Sp1 in cell cycle. We found that overexpression of Sp1 could repress the cell cycle progression, and stayed in G1/S phase. Recently we also used the Time‐lapse to observe the cell growth in living cells, and found the adeno‐GFP‐Sp1 infected cells could be inhibited in growth and led to death at last, but not occurred in adeno‐GFP infected cells. In the future, we will study which signal transduction pathway was involved in the death caused by overexpression of Sp1.