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FHL1 inhibits the growth of tongue squamous cell carcinoma cells via G1/S cell cycle arrest
- Source :
- Molecular medicine reports. 12(3)
- Publication Year :
- 2014
-
Abstract
- Four and a half LIM protein 1 (FHL1) has been characterized as a tumor suppressor in various types of tumor. However, the biological function and underlying mechanism of FHL1 in tongue squamous cell carcinoma (TSCC) remain to be elucidated. The present study demonstrated that FHL1 inhibits anchorage‑dependent and ‑independent growth of TSCC cells in vitro and tumor growth in nude mice, as determined by cell proliferation and soft agar assays. Knockdown of FHL1 with FHL1 small interfering RNA (siRNA) promoted tumor growth in nude mice. Mechanistically, flow cytometric analysis showed that knockdown of FHL1 promoted G1/S cell cycle progression. Furthermore, expression of cell cycle‑associated regulators, cyclin D and cyclin E, were detected by western blotting and reverse transcription‑quantitative polymerase chain reaction. Cyclin D and cyclin E were markedly elevated at both the protein and mRNA level in the FHL1 siRNA‑transfected cells. These results suggested that FHL1 has a tumor suppressive role in TSCC and that FHL1 may be a useful target for TSCC gene therapy.
- Subjects :
- Cancer Research
Small interfering RNA
Cyclin E
Cyclin D
Cell
Transplantation, Heterologous
Mice, Nude
Muscle Proteins
Biology
Real-Time Polymerase Chain Reaction
Biochemistry
Mice
Cell Movement
Cell Line, Tumor
Genetics
medicine
Animals
Humans
RNA, Small Interfering
Promoter Regions, Genetic
Molecular Biology
Gene knockdown
Mice, Inbred BALB C
Oncogene
Cell growth
Intracellular Signaling Peptides and Proteins
Cell cycle
DNA Methylation
LIM Domain Proteins
Molecular biology
G1 Phase Cell Cycle Checkpoints
Tongue Neoplasms
medicine.anatomical_structure
Oncology
S Phase Cell Cycle Checkpoints
biology.protein
Cancer research
Carcinoma, Squamous Cell
Molecular Medicine
RNA Interference
Subjects
Details
- ISSN :
- 17913004
- Volume :
- 12
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- Molecular medicine reports
- Accession number :
- edsair.doi.dedup.....1c91af3b50fb7574ec32d9d87fa51a55