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Background  Small cell lung carcinoma ( SCLC ) is characterized by a high rate of relapse and failure of chemotherapy because of the emergence of drug resistant cells.  N otch signaling controls carcinogenesis in several human malignancies and could be involved in the resistance of cells to several chemotherapeutic agents. Herein, we analyzed the role of  N otch1 signaling in the resistance of human  SCLC  cells to doxorubicin.    Methods  Small interfering ribonucleic acid technology was used to knock down ( KD )   Notch1   in  H 69 AR  and  SBC ‐3  SCLC  cells. We detected the effect of inhibiting  N otch1 on the expression of drug resistant related molecules: multidrug resistance‐associated protein ( MRP ‐1) and anti‐apoptotic factor B‐cell lymphoma‐2, as well as to cell adhesion molecule E‐cadherin, which contributes to the adhesion of  SCLC  cells to the extracellular matrix and confers chemoresistance in a process known as cell adhesion‐mediated drug resistance ( CAM‐DR) . We also observed the effect of  KD  Notch1   on cell survival under high concentrations of doxorubicin treated media.    Results   H 69 AR  and  SBC ‐3 cells expressed  N otch1 protein and grew as adherent aggregates, which confer resistance to high concentrations of doxorubicin. On inhibiting   Notch1  , we observed activation of the apoptotic pathway in cells, possibly resulting from the loss of  CAM‐DR  and, thus,  SBC ‐3 cells showed a loss of chemoresistant ability. However, in  H 69 AR  cells with  KD  Notch1  , the expression of  MRP ‐1 was increased and, thus, sustained the chemoresistant ability of cells.    Conclusion  The  N otch1 signaling pathway is involved in mediating the drug resistance phenotype of  SCLC  cells.

N otch1 controls cell chemoresistance in small cell lung carcinoma cells