INT99549
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Consistent with these results, enforced expression of the miR-222 can induce the thyroid papillary carcinoma cell line to progress to the S phase of the cell cycle, indicating that miR-222 negatively regulates p27Kip1 protein expression and cell cycle [24]. | |||||||||||||||
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Treatment of HT-29 cells with 5-FU resulted in decreased expressions of p21Cip1 and p27Kip1, and simultaneously in increased expression of CDK2. | |||||||||||||||
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Therefore, the up-regulation of p21Cip1 and p27Kip1 expressions in HT-29 cells induced by CQ, possibly contributed to the potentiation of the inhibitory effect of 5-FU, by promoting the cell cycle arrest to G0/G1 phase. | |||||||||||||||
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The pre-treatment of cells with CQ inhibited the down-regulation of p21Cip1 and p27Kip1 expressions induced by 5-FU and, on the other hand, inhibited the up-regulation of the expression of CDK2. | |||||||||||||||
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increase in the mRNA and protein expression of the Cyclin-dependent kinase inhibitor (Cki) p21waf1/cip1 and also an increase in protein expression only of p27kip1, another CKi. | |||||||||||||||
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in the transformed foci, and an overexpression of the CKi p27kip1 in | |||||||||||||||
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U50 488 produces a modest but significant decrease in viability associated with an arrest in the G0/G1 phase, but not antagonized by NorBNI and not associated with modulation of p21(Cip1), p27(Kip1) or p53 expression. | |||||||||||||||
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We further found that indomethacin, celecoxib and dexamethasone increased the mRNA and protein expressions of p27(kip1) and decreased those of cyclin D2 and p-cdk2 in hOBs. | |||||||||||||||
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Furthermore, the replenishment of PGE1, PGE2 or PGF2alpha did not reverse the effects of AIDs on proliferation and expressions of p27(kip1) and cyclin D2 in hOBs. | |||||||||||||||
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The p27kip1 expression was up-regulated by indomethacin, celecoxib and dexamethasone in both D1-cells and hBMSCs. | |||||||||||||||
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Ectopic overexpression of p21Cip1 or p27KiP1 markedly enhanced the apoptosis induced by sulindac sulfide. | |||||||||||||||
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in the transformed foci, and an overexpression of the CKi p27kip1 in | |||||||||||||||
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Treatment of HT-29 cells with 5-FU alone resulted in decreased expression of p21Cip1 and p27Kip1, and simultaneously in increased expression of CDK2, as detected by Western blot. | |||||||||||||||
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We found that both sulindac sulfide and TPA caused growth inhibition, cell cycle arrest in G0/G1 and increased levels of the cell cycle inhibitory proteins p21Cip1 and p27KiP1. | |||||||||||||||
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through increased expression of p21Cip1/Waf1, p27Kip1, and | |||||||||||||||
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Pre-treatment of cells with CQ inhibited the down-regulation of p21Cip1 and p27Kip1 expression induced by 5-FU and, on the other hand, decreased the expression of CDK2 (Fig. 7). | |||||||||||||||
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inhibition associated with G1 cell cycle arrest through increasing p27Kip1 protein expression
[140, 165167]. | |||||||||||||||
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We conclude that the changes in expressions of regulators of cell cycle (p27(kip1) and cyclin D2) and/or apoptosis (Bak and Bcl-XL) by AIDs may contribute to AIDs caused proliferation suppression and apoptosis in hOBs. | |||||||||||||||
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It has been reported that p44/42 MAPK phosphorylation is essential and sufficient for the increase in cdk2 [188, 189] and decrease in p27Kip1 expression [190, 191]. | |||||||||||||||
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Therefore, sulindac sulfide and related compounds may be useful in the treatment of leukemia and other neoplasms, especially when used together with agents that increase cellular levels of p21Cip1 or p27KiP1. | |||||||||||||||
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