[Silencing of the STAT3 gene expression activity and cancer cells metastatic potential at in vitro studies].
BACKGROUND
The STAT proteins are the mediators in the signal transduction in between extracellular environment and nucleus. Based on its own activity STATs regulate expression of genes involved in normal and pathological cellular processes. Constitutive STAT3 activation, the results of different cytokines inductions, has been shown in many primary human cancers. STAT3, as an oncogenic protein, plays an important role in the regulation of autonomous properties of cancer cells.


METHODS
In this study the effectiveness of the STAT3 gene expression activity silencing with RNA interference method was assessed. pSUPER.neo shRNA coding expression vector: shRNA-STAT3 and control vectors: shRNA-SCR, and pGFP were used. Effects of silencing of the examined gene was described as the phenotype changes of modulated HeLa (CCL-2) cancer cell line. To characterize modulated cancer cells phenotype changes two methods were applied: Wound Healing Assay and the stimulation to the apoptosis with anisomycin.


RESULTS
According to control cells, the silencing of the STAT3 gene expression activity reduced the mobility of modulated cells as well after 24 as after 48 hours after modulation. Also, after anisomycin stimulation the increasing in apoptotic modulated cell death was seen.


CONCLUSIONS
The inhibition of the activity of the STAT3 gene decreases HeLa cell migration, moreover the blocked STAT3 ability to the antyapoptotic gene expression activation leads to the increased susceptibility to apoptotic cell death.
Zakład Biotechnologii i Inzynierii Genetycznej, Slaski Uniwersytet Medyczny w Katowicach. m.poczeta@gmail.com
Marta
M
Poczeta
Zakład Biotechnologii i Inzynierii Genetycznej, Slaski Uniwersytet Medyczny w Katowicach.
Ilona
I
Bednarek
Zakład Biotechnologii i Inzynierii Genetycznej, Slaski Uniwersytet Medyczny w Katowicach.
Ewa
E
Nowak
Zakład Biotechnologii i Inzynierii Genetycznej, Slaski Uniwersytet Medyczny w Katowicach.
Anna
A
Galilejczyk
Zakład Biotechnologii i Inzynierii Genetycznej, Slaski Uniwersytet Medyczny w Katowicach.
Natalia
N
Gawlik
D000841:Anisomycin / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D020868:Gene Silencing; D006367:HeLa Cells / Q000502:physiology; D006801:Humans; D009362:Neoplasm Metastasis / Q000235:genetics*; D050796:STAT3 Transcription Factor / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics
D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D000841:Anisomycin