PMID- 26816546
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160128
LR  - 20181113
IS  - 1759-7706 (Print)
IS  - 1759-7714 (Electronic)
IS  - 1759-7706 (Linking)
VI  - 7
IP  - 1
DP  - 2016 Jan
TI  - Notch1 controls cell chemoresistance in small cell lung carcinoma cells.
PG  - 123-8
LID - 10.1111/1759-7714.12297 [doi]
AB  - 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. Notch 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 Notch1 signaling in the resistance of human SCLC 
      cells to doxorubicin. METHODS: Small interfering ribonucleic acid technology was 
      used to knock down (KD) Notch1 in H69AR and SBC-3 SCLC cells. We detected the 
      effect of inhibiting Notch1 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: H69AR and SBC-3 cells 
      expressed Notch1 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 H69AR cells with KD Notch1, the expression of MRP-1 was increased and, thus, 
      sustained the chemoresistant ability of cells. CONCLUSION: The Notch1 signaling 
      pathway is involved in mediating the drug resistance phenotype of SCLC cells.
FAU - Hassan, Wael Abdo
AU  - Hassan WA
AD  - Department of Pathology Faculty of Medicine Suez Canal University Ismailia Egypt; 
      Department of Pathology and Experimental Medicine Kumamoto University Graduate 
      School of Medical Sciences Kumamoto Japan.
FAU - Yoshida, Ryoji
AU  - Yoshida R
AD  - Department of Oral and Maxillofacial Surgery Kumamoto University Graduate School 
      of Medical Sciences Kumamoto Japan.
FAU - Kudoh, Shinji
AU  - Kudoh S
AD  - Department of Pathology and Experimental Medicine Kumamoto University Graduate 
      School of Medical Sciences Kumamoto Japan.
FAU - Kameyama, Hiroki
AU  - Kameyama H
AD  - Division of Pathology Kumamoto Health Science University Kumamoto Japan.
FAU - Hasegawa, Koki
AU  - Hasegawa K
AD  - Department of Pathology and Experimental Medicine Kumamoto University Graduate 
      School of Medical Sciences Kumamoto Japan.
FAU - Niimori-Kita, Kanako
AU  - Niimori-Kita K
AD  - Department of Pathology and Experimental Medicine Kumamoto University Graduate 
      School of Medical Sciences Kumamoto Japan.
FAU - Ito, Takaaki
AU  - Ito T
AD  - Department of Pathology and Experimental Medicine Kumamoto University Graduate 
      School of Medical Sciences Kumamoto Japan.
LA  - eng
PT  - Journal Article
DEP - 20150729
PL  - Singapore
TA  - Thorac Cancer
JT  - Thoracic cancer
JID - 101531441
PMC - PMC4718138
OTO - NOTNLM
OT  - Cell chemoresistance
OT  - Notch1 signaling
OT  - doxorubicin
OT  - small cell lung carcinoma (SCLC)
EDAT- 2016/01/28 06:00
MHDA- 2016/01/28 06:01
PMCR- 2016/01/01
CRDT- 2016/01/28 06:00
PHST- 2015/04/20 00:00 [received]
PHST- 2015/06/21 00:00 [accepted]
PHST- 2016/01/28 06:00 [entrez]
PHST- 2016/01/28 06:00 [pubmed]
PHST- 2016/01/28 06:01 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - TCA12297 [pii]
AID - 10.1111/1759-7714.12297 [doi]
PST - ppublish
SO  - Thorac Cancer. 2016 Jan;7(1):123-8. doi: 10.1111/1759-7714.12297. Epub 2015 Jul 
      29.