ABSTRACT
@#Objective To investigate the expression of long non－coding ＲNA SFTA1P in non small cell lung cancer ( NSCLC) and its biological function in NSCLC cell lines． Methods Quantitative real time polymerase chain reaction( qＲT－PCＲ) was used to detect the expression of SFTA1P in 18 pairs of NSCLC tissues and adjacent normal tissues． The expression of SFTA1P was detected by qＲT－PCＲ in five different NSCLC cell lines ( A549，SPCA1，H460，H1975 and H1299) and one normal lung epithelial cell line ( HBE) ． The overexpression vector of SFTA1P was designed and constructed． The overex- pressed cell line was constructed by transfection，the effects of overexpression of SFTA1P on proliferation， invasion and migration of NSCLC cells were detected by CCK－8 assay and transwell assay． Ｒesults The expression of SFTA1P in NSCLC tissues was lower than that of adjacent normal tissues ( t = 2. 158，P = 0. 043) ． SFTA1P expression was detected in 5 strains of NSCLC cell lines and normal lung epithelial cell line． The expression of SFTA1P was the lowest in A549 and H460 cell lines ( t = 5. 769，P = 0. 004; t = 5. 772，P= 0. 004) ，and the highest in H1299 and H1975 cell lines ( t = 22. 248，P＜0. 001; t = 11. 814，P ＜0. 001) ． SFTA1P overexpression cell models were successfully constructed using A549 and H460 cell lines( all P＜0．05) ． The overexpression of SFTA1P could inhibit proliferation，invasion and migration of H460 and A549 cells ( ( all P ＜ 0． 05) ． Conclusions SFTA1P can affect the biological functions of NSCLC cells by inhibiting the proliferation，migration and invasion． SFTA1P may play a role as a tumor suppressor gene in tumorigenesis and development．
ABSTRACT
<p><b>AIM</b>To explore the relationship between expression of signal transduction and activators of transcription 3 (STAT3) gene and proliferation of rat pulmonary arterial smooth muscle cells (PASMCs) under hypoxia conditions.</p><p><b>METHODS</b>After primarily cultured rat PASMCs was treated with AG490 and then exposed to hypoxia, the tyrosine-phosphorylated STAT3 protein were detected at 2 h, 6 h, 12 h, 16 h, 24 h of exposure to hypoxia by semi-quantitive RT-PCR (sqRT-PCR) and Western blot respectively. The expression of c-myc mRNA was analyzed by sqRT-PCR. 3H-TdR incorporation was used to detect the cell proliferation.</p><p><b>RESULTS</b>The level of tyrosine-phosphorylated STAT3 increased at 6 h and peaked at 12 h. The expression of c-myc mRNA increased after 2 h of hypoxia and reached maximal level at 4 h, then declined at 6 h and to the basal levels at 12 h. With the prolonging of hypoxia time, 3H-TdR incorporation in PASMC under hypoxia conditions was significantly higher. AG490 inhibited proliferation of PASMCs by preventing STAT3 tyrosine phosphorylation and the expression of c-myc under hypoxia conditions.</p><p><b>CONCLUSION</b>(1) The activation of STAT3 and c-myc gene might play an important role in the early stage of hypoxia-induced PASMCs proliferation. (2) STAT3 upregulated the expression of c-myc during the proliferation of PASMCs induced by hypoxia.</p>