Transcriptional characterization of the notch signaling pathway in rodent multipotent adult progenitor cells

Hajdú, Melinda; Luttun, Aernout; Pelacho, Beatriz; Burns, Terry C.; Chase, Lucas G.; Gutiérrez-Pérez, María; Jiang, Yuehua; Lenvik, Todd; Vas, Virág; Uher, Ferenc; Sebestyén, Anna; Verfaillie, Cathérine

doi:10.1007/bf02940309

Cited by 7 publications

(5 citation statements)

References 51 publications

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“…The CBF1‐dependent Notch signal pathway can activate its own expression [59]. Several studies showed that the activation of one Notch receptor can induce or repress the other Notch signalings [60–64]. In addition, each of the 4 Notch receptors may have a distinct target sequence selectivity [65] and play a differential biological function.…”

Section: Discussionmentioning

confidence: 99%

Notch2‐induced COX‐2 expression enhancing gastric cancer progression

Tseng¹,

Tsai

Tseng

et al. 2011

Molecular Carcinogenesis

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Gastric carcinoma is one of the most common and mortal types of malignancy worldwide. To date, the mechanisms controlling its aggressiveness are not yet fully understood. Notch signal pathway can function as either an oncogene or a tumor suppressor in tumorigenesis. Four members (Notch1-4) of Notch receptors were found in mammals and each exhibits distinct roles in tumor progression. Previous study showed that the activated Notch1 receptor promoted gastric cancer progression through cyclooxygenase-2 (COX-2). This study addressed whether Notch2 signal pathway is also involved in gastric cancer progression. Constitutive expression of Notch2 intracellular domain (N2IC), the activated form of Notch2 receptor, promoted both cell proliferation and xenografted tumor growth of human stomach adenocarcinoma SC-M1 cells. The colony formation, migration, invasion, and wound-healing abilities of SC-M1 cells were enhanced by N2IC expression, whereas these abilities were suppressed by Notch2 knockdown. Similarly, Notch2 knockdown inhibited cancer progressions of AGS and AZ521 gastric cancer cells. Expression of N2IC also caused epithelial-mesenchymal transition in SC-M1 cells. Furthermore, N2IC bound to COX-2 promoter and induced COX-2 expression through a CBF1-dependent manner in SC-M1 cells. The ability of N2IC to enhance tumor progression in SC-M1 cells was suppressed by knockdown of COX-2 or treatment with NS-398, a COX-2 inhibitor. Moreover, the suppression of tumor progression by Notch2 knockdown in SC-M1 cells was reversed by exogenous COX-2 or its major enzymatic product PGE(2) . Taken together, this study is the first to demonstrate that the Notch2-COX-2 signaling axis plays an important role in controlling gastric cancer progression.

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Section: Discussionmentioning

confidence: 99%

Notch2‐induced COX‐2 expression enhancing gastric cancer progression

Tseng¹,

Tsai

Tseng

et al. 2011

Molecular Carcinogenesis

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“…There are response elements in the upstream of Notch gene that can potentially bind with CBF1 to activate itself by Notch signal pathway [Ganapati et al, 2007]. The regulatory feedback loops of Notch signaling are present to induce expressions of Notch1 and Notch3 mRNAs [Hajdu et al, 2007]. Notch1 receptor also induces and cooperates with Notch4 receptor [Krebs et al, 2000;Weijzen et al, 2002].…”

Section: Discussionmentioning

confidence: 99%

The autonomous notch signal pathway is activated by baicalin and baicalein but is suppressed by niclosamide in K562 cells

Wang¹,

Ku²,

Liang

et al. 2009

J of Cellular Biochemistry

101

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The Notch signaling pathway plays important roles in a variety of cellular processes. Aberrant transduction of Notch signaling contributes to many diseases and cancers in humans. The Notch receptor intracellular domain, the activated form of Notch receptor, is extremely difficult to detect in normal cells. However, it can activate signaling at very low protein concentration to elicit its biological effects. In the present study, a cell based luciferase reporter gene assay was established in K562 cells to screen drugs which could modulate the endogenous CBF1-dependent Notch signal pathway. Using this system, we found that the luciferase activity of CBF1-dependent reporter gene was activated by baicalin and baicalein but suppressed by niclosamide in both dose- and time-dependent manners. Treatment with these drugs modulated endogenous Notch signaling and affected mRNA expression levels of Notch1 receptor and Notch target genes in K562 cells. Additionally, erythroid differentiation of K562 cells was suppressed by baicalin and baicalein yet was promoted by niclosamide. Colony-forming ability in soft agar was decreased after treatment with baicalin and baicalein, but was not affected in the presence of niclosamide. Thus, modulation of Notch signaling after treatment with any of these three drugs may affect tumorigenesis of K562 cells suggesting that these drugs may have therapeutic potential for those tumors associated with Notch signaling. Taken together, this system could be beneficial for screening of drugs with potential to treat Notch signal pathway-associated diseases.

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“…Relative quantitation was performed by taking the difference (DCt) between the DCt of GAPDH and DCt of each target transcript and computing the DCt. They were amplified as follows: 95 C for 10 min, followed by 50 cycles at 95 C for 15 s and 60 C for 30 s ( Köhler et al, 2004;Hajdu et al, 2007). The reactions were done in triplicate in 3 separate experiments.…”

Section: Real-time Polymerase Chain Reactionmentioning

confidence: 99%

Crucial role of Notch signaling in osteogenic differentiation of periodontal ligament stem cells in osteoporotic rats

et al. 2014

Cell Biology International

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Estrogen deficiency-induced osteoporosis typically occurs in postmenopausal women and has been strongly associated with periodontal diseases. Periodontal ligament stem cells (PDLSCs) isolated from the periodontal ligament can differentiate into many types of specialized cells, including osteoblast-like cells that contribute to periodontal tissue repair. The Notch signaling pathway is highly conserved and associated with self-renewal potential and cell-fate determination. Recently, several studies have focused on the relationship between Notch signaling and osteogenic differentiation. However, the precise mechanisms underlying this relationship are largely unknown. We have successfully isolated PDLSCs from both ovariectomized (OVX) and sham-operated rats. Both the mRNA and protein levels of Notch1 and Jagged1 were upregulated when PDLSCs were cultured in osteogenic induction media. Mineralization assays showed decreased calcium deposits in OVX-PDLSCs treated with a γ-secretase inhibitor compared with control cells. Thus Notch signaling is important in maintaining the osteogenic differentiation of PDLSCs in osteoporotic rats, which help in the development of a potential therapeutic strategy for periodontal disease in postmenopausal women.

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Transcriptional characterization of the notch signaling pathway in rodent multipotent adult progenitor cells

Cited by 7 publications

References 51 publications

Notch2‐induced COX‐2 expression enhancing gastric cancer progression

Notch2‐induced COX‐2 expression enhancing gastric cancer progression

The autonomous notch signal pathway is activated by baicalin and baicalein but is suppressed by niclosamide in K562 cells

Crucial role of Notch signaling in osteogenic differentiation of periodontal ligament stem cells in osteoporotic rats

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