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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

Notch-1 siRNA inhibited cell proliferation and induced apoptosis in A549 cells. (A) MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (B) Flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells. Data expressed as mean± s.e.m.; *P<0.05 and **P<0.01 compared to control siRNA-treated cells.
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BIO017798F5: Notch-1 siRNA inhibited cell proliferation and induced apoptosis in A549 cells. (A) MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (B) Flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells. Data expressed as mean± s.e.m.; *P<0.05 and **P<0.01 compared to control siRNA-treated cells.

Mentions: Our study suggested that leptin knockdown inactivated Notch signaling, which played a role in proliferation and apoptosis in NSCLC cells. We sought to determine whether the inhibition of Notch signaling by Notch-1 siRNA suppressed cell proliferation and induced apoptosis in A549 cells. MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (P<0.05) (Fig. 5A). As shown in Fig. 5B, flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells (P<0.01). Additionally, the expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells (Fig. 5C).Fig. 5.


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)

Notch-1 siRNA inhibited cell proliferation and induced apoptosis in A549 cells. (A) MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (B) Flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells. Data expressed as mean± s.e.m.; *P<0.05 and **P<0.01 compared to control siRNA-treated cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

BIO017798F5: Notch-1 siRNA inhibited cell proliferation and induced apoptosis in A549 cells. (A) MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (B) Flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells. (C) The expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells. Data expressed as mean± s.e.m.; *P<0.05 and **P<0.01 compared to control siRNA-treated cells.
Mentions: Our study suggested that leptin knockdown inactivated Notch signaling, which played a role in proliferation and apoptosis in NSCLC cells. We sought to determine whether the inhibition of Notch signaling by Notch-1 siRNA suppressed cell proliferation and induced apoptosis in A549 cells. MTT assay showed that the growth rate of the Notch-1 siRNA-treated cells was significantly lower than the control siRNA-treated cells after transfection for 48 h (P<0.05) (Fig. 5A). As shown in Fig. 5B, flow cytometry analysis revealed that Notch-1 siRNA significantly induced apoptosis in A549 cells (P<0.01). Additionally, the expression levels of Ki67 and Bcl-2 were markedly downregulated and Bax expression was upregulated in Notch-1 siRNA-treated cells compared with control siRNA-treated cells (Fig. 5C).Fig. 5.

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