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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

Inactivation of JAK/STAT3 signaling pathway suppressed cell viability and induced apoptosis in A549 cells. Cells were treated with 1 μM JAK/STAT3signaling pathway inhibitor, JSI-124 for 12 h. (A) Cell proliferation was measured by MTT assay. JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group. (B) Flow cytometry analysis was used to detect the apoptosis in A549 after JSI-124 treatment. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group. Data expressed as mean±s.e.m.; *P<0.05 and **P<0.01 compared to control group.
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BIO017798F6: Inactivation of JAK/STAT3 signaling pathway suppressed cell viability and induced apoptosis in A549 cells. Cells were treated with 1 μM JAK/STAT3signaling pathway inhibitor, JSI-124 for 12 h. (A) Cell proliferation was measured by MTT assay. JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group. (B) Flow cytometry analysis was used to detect the apoptosis in A549 after JSI-124 treatment. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group. Data expressed as mean±s.e.m.; *P<0.05 and **P<0.01 compared to control group.

Mentions: A549 cells were treated with 1 μM JAK/STAT3 signaling pathway inhibitor, JSI-124, for 12 h to further understand JAK/STAT3 signaling in leptin knockdown-induced cell proliferation inhibition and apoptosis induction in NSCLC cells. As shown in Fig. 6A, JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group (P<0.05). Results from flow cytometry analysis showed that JSI-124 treatment significantly increased apoptosis in A549 cells compared with control group (P<0.01) (Fig. 6B). Furthermore, the expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group (Fig. 6C).Fig. 6.


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)

Inactivation of JAK/STAT3 signaling pathway suppressed cell viability and induced apoptosis in A549 cells. Cells were treated with 1 μM JAK/STAT3signaling pathway inhibitor, JSI-124 for 12 h. (A) Cell proliferation was measured by MTT assay. JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group. (B) Flow cytometry analysis was used to detect the apoptosis in A549 after JSI-124 treatment. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group. Data expressed as mean±s.e.m.; *P<0.05 and **P<0.01 compared to control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

BIO017798F6: Inactivation of JAK/STAT3 signaling pathway suppressed cell viability and induced apoptosis in A549 cells. Cells were treated with 1 μM JAK/STAT3signaling pathway inhibitor, JSI-124 for 12 h. (A) Cell proliferation was measured by MTT assay. JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group. (B) Flow cytometry analysis was used to detect the apoptosis in A549 after JSI-124 treatment. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group. Data expressed as mean±s.e.m.; *P<0.05 and **P<0.01 compared to control group.
Mentions: A549 cells were treated with 1 μM JAK/STAT3 signaling pathway inhibitor, JSI-124, for 12 h to further understand JAK/STAT3 signaling in leptin knockdown-induced cell proliferation inhibition and apoptosis induction in NSCLC cells. As shown in Fig. 6A, JSI-124 treatment significantly inhibited the growth of A549 cells compared with control group (P<0.05). Results from flow cytometry analysis showed that JSI-124 treatment significantly increased apoptosis in A549 cells compared with control group (P<0.01) (Fig. 6B). Furthermore, the expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in JSI-124-treated cells compared with control group (Fig. 6C).Fig. 6.

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