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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 by leptin-targeted siRNA reduced cell proliferation in NSCLC A549 and 95D cells. (A,C) Growth curves calculated for A549 and 95D cells treated with leptin siRNA and control siRNA. (B,D) Ki67 expression A549 and 95D cells treated with siRNA transfection. Western blot analysis showed that Ki67 expression in cells treated with leptin siRNA was significantly lower than that of cells treated with control siRNA. Data expressed as mean± s.e.m.; *P<0.05 compared to control siRNA-treated cells.
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BIO017798F2: Silencing of leptin by leptin-targeted siRNA reduced cell proliferation in NSCLC A549 and 95D cells. (A,C) Growth curves calculated for A549 and 95D cells treated with leptin siRNA and control siRNA. (B,D) Ki67 expression A549 and 95D cells treated with siRNA transfection. Western blot analysis showed that Ki67 expression in cells treated with leptin siRNA was significantly lower than that of cells treated with control siRNA. Data expressed as mean± s.e.m.; *P<0.05 compared to control siRNA-treated cells.

Mentions: To measure the effect of leptin knockdown on NSCLC cell viability, MTT assay was used to determine growth activity of A549 and 95D cells transfected with leptin siRNA or control siRNA (Fig. 2A,C). The results showed that all of the two cell lines transfected with leptin siRNA displayed lower proliferation rates compared with cells with control siRNA. Moreover, in accordance with the cell viability, the protein expression of Ki67 in leptin siRNA-transfected cells also decreased significantly compared with control siRNA-transfected cells (Fig. 2B,D).Fig. 2.


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 by leptin-targeted siRNA reduced cell proliferation in NSCLC A549 and 95D cells. (A,C) Growth curves calculated for A549 and 95D cells treated with leptin siRNA and control siRNA. (B,D) Ki67 expression A549 and 95D cells treated with siRNA transfection. Western blot analysis showed that Ki67 expression in cells treated with leptin siRNA was significantly lower than that of cells treated with control siRNA. Data expressed as mean± s.e.m.; *P<0.05 compared to control siRNA-treated cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

BIO017798F2: Silencing of leptin by leptin-targeted siRNA reduced cell proliferation in NSCLC A549 and 95D cells. (A,C) Growth curves calculated for A549 and 95D cells treated with leptin siRNA and control siRNA. (B,D) Ki67 expression A549 and 95D cells treated with siRNA transfection. Western blot analysis showed that Ki67 expression in cells treated with leptin siRNA was significantly lower than that of cells treated with control siRNA. Data expressed as mean± s.e.m.; *P<0.05 compared to control siRNA-treated cells.
Mentions: To measure the effect of leptin knockdown on NSCLC cell viability, MTT assay was used to determine growth activity of A549 and 95D cells transfected with leptin siRNA or control siRNA (Fig. 2A,C). The results showed that all of the two cell lines transfected with leptin siRNA displayed lower proliferation rates compared with cells with control siRNA. Moreover, in accordance with the cell viability, the protein expression of Ki67 in leptin siRNA-transfected cells also decreased significantly compared with control siRNA-transfected cells (Fig. 2B,D).Fig. 2.

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