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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

Silencing of leptin inactivated the Notch and JAK/STAT3 signaling pathways. In both A549 (A) and 95D (B) cells, knockdown of leptin led to decreased levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2 and p-STAT3 but not total-JAK1 (t-JAK1), t-JAK2, and t-STAT3.
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BIO017798F4: Silencing of leptin inactivated the Notch and JAK/STAT3 signaling pathways. In both A549 (A) and 95D (B) cells, knockdown of leptin led to decreased levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2 and p-STAT3 but not total-JAK1 (t-JAK1), t-JAK2, and t-STAT3.

Mentions: Expression levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2, p-STAT3, total-JAK1 (t-JAK1), t-JAK2, and t-STAT3 were measured by western blot to evaluate the effect of leptin knockdown on the Notch and JAK/STAT3 signaling pathways (Fig. 4A,B). In both A549 and 95D cells, leptin siRNA treatment for 48 h significantly downregulated the expression of Notch-1, p-JAK1, p-JAK2, and p-STAT3 but not t-JAK1, t-JAK2, and t- STAT3 compared with control siRNA treatment. The results indicated that knockdown of leptin led to inactivation of both the Notch and JAK/STAT3 signaling pathways in NSCLC cells.Fig. 4.


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)

Silencing of leptin inactivated the Notch and JAK/STAT3 signaling pathways. In both A549 (A) and 95D (B) cells, knockdown of leptin led to decreased levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2 and p-STAT3 but not total-JAK1 (t-JAK1), t-JAK2, and t-STAT3.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

BIO017798F4: Silencing of leptin inactivated the Notch and JAK/STAT3 signaling pathways. In both A549 (A) and 95D (B) cells, knockdown of leptin led to decreased levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2 and p-STAT3 but not total-JAK1 (t-JAK1), t-JAK2, and t-STAT3.
Mentions: Expression levels of Notch-1, phosphorylated-JAK1 (p-JAK1), p-JAK2, p-STAT3, total-JAK1 (t-JAK1), t-JAK2, and t-STAT3 were measured by western blot to evaluate the effect of leptin knockdown on the Notch and JAK/STAT3 signaling pathways (Fig. 4A,B). In both A549 and 95D cells, leptin siRNA treatment for 48 h significantly downregulated the expression of Notch-1, p-JAK1, p-JAK2, and p-STAT3 but not t-JAK1, t-JAK2, and t- STAT3 compared with control siRNA treatment. The results indicated that knockdown of leptin led to inactivation of both the Notch and JAK/STAT3 signaling pathways in NSCLC cells.Fig. 4.

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