Limits...
Downregulation of leptin inhibits growth and induces apoptosis of lung cancer cells via the Notch and JAK/STAT3 signaling pathways.

Zheng XJ, Yang ZX, Dong YJ, Zhang GY, Sun MF, An XK, Pan LH, Zhang SL - Biol Open (2016)

Bottom Line: Leptin expression was significantly increased in NSCLC cell lines compared with normal human bronchial epithelial cell HBE.Furthermore, gene silencing of Notch signaling with Notch-1 siRNA or inhibition of JAK/STAT3 signaling by JSI-124, an inhibitor of STAT3, resulted in proliferation inhibition and apoptosis induction in NSCLC A549 cells.Our findings suggested that leptin knockdown could become a new approach for the prevention of lung cancer progression, which is likely to be mediated at least partially by inactivation of the Notch and JAK/STAT3 signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, The First Affiliated Hospital of Henan University, Kaifeng, Henan Province 475000, China.

No MeSH data available.


Related in: MedlinePlus

Detection of leptin expression in NSCLC cell lines. (A) Levels of leptin expression in HBE, 95C, H460, 95D, A549, H1299 and SPC-A-1 cells were determined by qRT-PCR. (B) Western blot analysis was employed to detect the protein expression levels of leptin in NSCLC cell lines. Data expressed as mean± s.e.m.; *P<0.05 compared to HBE cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4920192&req=5

BIO017798F1: Detection of leptin expression in NSCLC cell lines. (A) Levels of leptin expression in HBE, 95C, H460, 95D, A549, H1299 and SPC-A-1 cells were determined by qRT-PCR. (B) Western blot analysis was employed to detect the protein expression levels of leptin in NSCLC cell lines. Data expressed as mean± s.e.m.; *P<0.05 compared to HBE cells.

Mentions: To measure the biological roles of leptin in NSCLC cells, we first determined the expression of leptin in NSCLC cell lines including 95C, H460, 95D, A549, H1299, SPC-A-1 and in normal human bronchial epithelial cell HBE by qRT-PCR and western blot. The results showed that the mRNA expression of leptin was significantly increased in six NSCLC cell lines compared with HBE (Fig. 1A). Similarly, western blot analysis showed that compared with HBE cells protein expression levels of leptin was significantly elevated in NSCLC cell lines (Fig. 1B).Fig. 1.


Downregulation of leptin inhibits growth and induces apoptosis of lung cancer cells via the Notch and JAK/STAT3 signaling pathways.

Zheng XJ, Yang ZX, Dong YJ, Zhang GY, Sun MF, An XK, Pan LH, Zhang SL - Biol Open (2016)

Detection of leptin expression in NSCLC cell lines. (A) Levels of leptin expression in HBE, 95C, H460, 95D, A549, H1299 and SPC-A-1 cells were determined by qRT-PCR. (B) Western blot analysis was employed to detect the protein expression levels of leptin in NSCLC cell lines. Data expressed as mean± s.e.m.; *P<0.05 compared to HBE cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4920192&req=5

BIO017798F1: Detection of leptin expression in NSCLC cell lines. (A) Levels of leptin expression in HBE, 95C, H460, 95D, A549, H1299 and SPC-A-1 cells were determined by qRT-PCR. (B) Western blot analysis was employed to detect the protein expression levels of leptin in NSCLC cell lines. Data expressed as mean± s.e.m.; *P<0.05 compared to HBE cells.
Mentions: To measure the biological roles of leptin in NSCLC cells, we first determined the expression of leptin in NSCLC cell lines including 95C, H460, 95D, A549, H1299, SPC-A-1 and in normal human bronchial epithelial cell HBE by qRT-PCR and western blot. The results showed that the mRNA expression of leptin was significantly increased in six NSCLC cell lines compared with HBE (Fig. 1A). Similarly, western blot analysis showed that compared with HBE cells protein expression levels of leptin was significantly elevated in NSCLC cell lines (Fig. 1B).Fig. 1.

Bottom Line: Leptin expression was significantly increased in NSCLC cell lines compared with normal human bronchial epithelial cell HBE.Furthermore, gene silencing of Notch signaling with Notch-1 siRNA or inhibition of JAK/STAT3 signaling by JSI-124, an inhibitor of STAT3, resulted in proliferation inhibition and apoptosis induction in NSCLC A549 cells.Our findings suggested that leptin knockdown could become a new approach for the prevention of lung cancer progression, which is likely to be mediated at least partially by inactivation of the Notch and JAK/STAT3 signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, The First Affiliated Hospital of Henan University, Kaifeng, Henan Province 475000, China.

No MeSH data available.


Related in: MedlinePlus