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KLF6: mutational analysis and effect on cancer cell proliferation
Dong Yin1, Naoki Komatsu, Carl W Miller
1Division of Hematology and Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA 90048, USA. dong.yin@cshs.org
International Journal of Oncology
|December 5, 2006
Summary
Kruppel-like factor 6 (KLF6) alterations were found in brain and lung cancers. Some KLF6 mutations in brain tumors impair its tumor suppressor function, suggesting KLF6 dysfunction contributes to brain cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Kruppel-like factor 6 (KLF6) is a transcription factor implicated as a tumor suppressor in various cancers.
- The role of KLF6 alterations in non-small cell lung cancer (NSCLC) and brain tumors requires further investigation.
Purpose of the Study:
- To investigate the frequency and functional impact of KLF6 gene alterations in NSCLC and brain tumors.
- To assess KLF6 expression levels in normal brain tissue versus glioma samples.
Main Methods:
- Single strand conformation polymorphism (PCR-SSCP) and DNA sequencing were used to detect KLF6 alterations in tumor samples and cell lines.
- Functional assays involved transfecting a glioblastoma (GBM) cell line with wild-type and mutant KLF6 variants.
- Real-time RT-PCR was employed to quantify KLF6 expression levels.
Main Results:
- KLF6 coding region alterations were identified in 10% of brain tumors, 8% of NSCLC, and 4% of cancer cell lines.
- Nucleotide changes upstream of the KLF6 start codon were observed in 45% of brain tumors.
- Wild-type KLF6 and specific mutants (deleted exon 3, E30G) reduced GBM cell growth, while other mutants (S92R, P183L, A276G) did not.
- KLF6 expression was significantly lower in glioma samples compared to normal brain tissue.
Conclusions:
- KLF6 alterations occur in brain and lung cancers, with some mutations affecting its tumor suppressor activity in gliomas.
- Germline polymorphisms account for all observed KLF6 changes in lung cancer.
- Decreased KLF6 expression and functional impairment of its tumor suppressor role may contribute to brain oncogenesis.
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