ABSTRACT
<p><b>BACKGROUND</b>To investigate the expression of the SOCS3 gene and its effect on proliferation of A549 cells.</p><p><b>METHODS</b>A549 cells were cotransfected with pEFSOCS3 and pSV2neo by liposome, then G418 was used to screen the positive cells. Expression of SOCS3 mRNA and protein was detected by RT-PCR and immunocytochemistry respectively before and after transfection. MTT assay was used to detect the cell growth. Flow cytometric DNA analysis was used to determine the cell cycle.</p><p><b>RESULTS</b>RT-PCR and immunocytochemistry showed that no expression of SOCS3 mRNA and protein was detected in A549 cells before transfection, but a stable expression of SOCS3 gene was observed after transfection with SOCS3 gene. Compared with control group, growth of A549 cells transfected with SOCS3 gene was significantly suppressed, with a suppressive rate of 41.07%. The cells at G₀/G₁ cell phases increased, and those at S and G₂/M phases decreased significantly after transfection.</p><p><b>CONCLUSIONS</b>SOCS3 protein might inhibit the proliferation of A549 cells by negatively regulating cellular signal pathways.</p>
ABSTRACT
<p><b>BACKGROUND</b>To determine the inhibitory effect of antisense peptide nucleic acids (PNA) of telomerase on the growth of lung cancer cell lines.</p><p><b>METHODS</b>The synthesized modified antisense PNAs of telomerase were transfected into the lung cancer cell lines A549 and NCI-H446 respectively by lipofectamine transfection. Telomerase activity was detected by RT-PCR-ELLISA, and the cell counts were determined by MTT.</p><p><b>RESULTS</b>Seventy two hours after transfection with antisense PNAs of telomerase, telomerase activity (A450 value) of A549 and NCI-H446 were down regulated from 0.582 ±0.039, 0.571±0.043 to 0.294±0.048 ( P < 0.01), 0.276±0.051 ( P < 0.01) respectively, and alive cell counts (A580 value) of them from 0.485± 0.009 , 0.513±0.015 to 0.191±0.027 ( P < 0.01), 0.138±0.046 ( P < 0.01) respectively. The growth of two lung cancer cell lines were significantly inhibited.</p><p><b>CONCLUSIONS</b>Antisense PNA of telomerase might inhibit not only the telomerase activity, but also the growth of lung cancer cell lines in vitro.</p>
ABSTRACT
<p><b>BACKGROUND</b>To evaluate the clinical significance of telomerase activity in lung cancer and to investigate the possibility of telomerase as cancer marker for lung cancer.</p><p><b>METHODS</b>The activity of telomerase was investigated by TRAP-PCR-ELISA in lung cancer tissues and corresponding adjacent noncancerous tissues obtained from resected specimens of 48 patients with lung cancer and 42 specimens of benign pulmonary lesions were examined simultaneously.</p><p><b>RESULTS</b>Telomerase activity was detected in 42 (87.5%) of the 48 tumors and only 4 (8.3%) of the 48 adjacent noncancerous lung tissue samples (Chi-Square=13.029, P < 0.01), but in none of 42 specimens of benign pulmonary lesions (Chi-Square=14.016, P < 0.01). Correlation with pathological parameters showed that the expression of telomerase activity was associated with lymph node metastasis (93.5% vs 76.4% , Chi-Square=63.511, P < 0.01), but not with histological type, location and differenciated grade of tumor.</p><p><b>CONCLUSIONS</b>Telomerase activation correlates with the carcinogenesis and aggressiveness of lung cancer. Telomerase might be one of the important diagnostic and prognostic factors in patients with lung cancer.</p>
ABSTRACT
Objective To study the 4 977 bp deletion of mitochondrial DNA in lung cancer, paraneoplastic tissue and normal lung tissue from non-lung cancer subjects and its significance in the development of cancer. Methods Lung cancer tissues and paraneoplastic tissues from 37 non-small lung cancer patients, and normal lung tissues from 20 patients without lung cancer were analyzed by long PCR technique. Results Mitochondrial DNA 4 977 bp deletion was detected in 54.1%(20/37) of lung cancer tissues, 59.5%(22/37) of paraneoplastic tissues and 30.0%(6/30) of normal lung tissues. The correlation between 4 977 bp deletion and age, smoking was present in our data. Conclusion Mitochondrial DNA 4 977 bp deletion, which may reflect the environmental and genetic influences during tumor progression, is not specific to lung cancer and unlikely to play an important role in carcinogenesis.
ABSTRACT
Objective To investigate the variations of mtDNA from high and low metastatic mouse hepatocarcinoma cell sublines Hca-F and Hca-P, and the relationship between mutations of mtDNA and carcinogenesis. Methods The variations of D-loop, ND3 and tRNA Met+Glu+Ile gene fragments of mtDNA from Hca-F and Hca-P cells were analyzed by PCR-RFLP and sequencing techniques. Results No amplification fragment length polymorphism and restriction fragment length polymorphism were observed in tRNA Met+Glu+Ile , ND3 and D-loop of mtDNA from the 2 cell sublines. Sequence difference between these 2 cell sublines were found in mtDNA D-loop region by sequencing. Conclusions Genetic alteration of mtDNA non-coding region in tumors, which may reflect the environmental and genetic influences operative during tumor progression, can be linked to their tumorigenic phenotype.