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Effects of NOTCH1 signaling inhibitor ?-secretase inhibitor II on growth of cancer stem cells.

ABSTRACT: The present study aimed to observe the effect of the Notch1 signaling inhibitor ?-secretase inhibitor II (GSI II) on the growth and differentiation of tumor cells. The tumor cell line U87 was grown in serum-free media, and cell growth was evaluated using immunofluorescence. Single-cell wall-adherent growing conditions were prepared, GSI II was added, and the differentiation and growth of single tumor cells was evaluated. Immunofluorescence demonstrated positive results for the expression of Nestin and cluster of differentiation 133. The cell proliferation rate was reduced following the addition of GSI II (P<0.05). GSI II may significantly inhibit the proliferation and differentiation of U87 tumor stem cells.

SUBMITTER: Ding X

PROVIDER: S-EPMC6202534 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Effects of NOTCH1 signaling inhibitor γ-secretase inhibitor II on growth of cancer stem cells.

Ding Xiaodong X Ding Changqing C Wang Fei F Deng Wenshuai W Yu Mingming M Meng Qinghai Q Sun Peng P

Oncology letters 20180903 5

The present study aimed to observe the effect of the Notch1 signaling inhibitor γ-secretase inhibitor II (GSI II) on the growth and differentiation of tumor cells. The tumor cell line U87 was grown in serum-free media, and cell growth was evaluated using immunofluorescence. Single-cell wall-adherent growing conditions were prepared, GSI II was added, and the differentiation and growth of single tumor cells was evaluated. Immunofluorescence demonstrated positive results for the expression of Nest ...[more]

PMID: 30405755

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Project description:BackgroundTraumatic heterotopic ossification (THO) is a devastating sequela following traumatic injuries and orthopedic surgeries. To date, the exact molecular mechanism of THO formation is still unclear, which hinders the development of effective treatments. The process of THO formation is believed to recapitulate a series of spatiotemporal cellular and signaling events that occur during skeletal development. The Notch signaling pathway is a critical genetic regulator in embryological bone development and fracture healing. However, few data are available concerning whether Notch signaling regulates THO development and maturation.MethodsWe firstly detected the expressions of Notch target genes in both mouse and human THO samples with quantitative RT-PCR and immunohistochemistry (IHC). Then, tissue-resident mesenchymal progenitor cells (TMPCs) were isolated, and the abilities of the proliferation and osteogenic and chondrogenic differentiation of TMPCs were examined under the intervention of the gamma-secretase inhibitor-DAPT at different time points. Finally, DAPT was also administrated in THO mice by burn and Achilles tenotomy injury, and ectopic cartilage and bone formation were monitored by histology and micro-CT.ResultsSeveral Notch target genes were upregulated in both mouse and human THO tissues. Sustained Notch signaling inhibition by DAPT reduced proliferation, osteogenic and chondrogenic differentiation of TMPCs in a time-dependent manner. Moreover, DAPT administration within 3 weeks could inhibit ectopic cartilage and bone formation in a mouse THO model without affecting the total body bone mass.ConclusionsThe Notch signaling serves as an important therapeutic target during THO formation. And sustained gamma-secretase inhibition by DAPT has great potential in repressing chondrogenic and osteogenic differentiation of TMPCs, as well as inhibited ectopic cartilage and bone formation in vivo.The translational potential of this articleSustained Notch inhibition via systemic DAPT (or other similar gamma-secretase inhibitors) administration has promising clinical utility for inhibiting THO formation, providing new insight into THO prophylaxis and treatment.

Dataset Information

Effects of NOTCH1 signaling inhibitor ?-secretase inhibitor II on growth of cancer stem cells.

Publications

Effects of NOTCH1 signaling inhibitor γ-secretase inhibitor II on growth of cancer stem cells.

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