INT99549

Context Info Confidence 0.75 First Reported 2001 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 30 Total Number 30 Disease Relevance 17.00 Pain Relevance 5.15

cytosol (CDKN1B) endosome (CDKN1B) nucleoplasm (CDKN1B) nucleus (CDKN1B) cell cycle (CDKN1B) kinase activity (CDKN1B)

Anatomy Link Frequency HT-29 3 thyroid 1 CDKN1B (Homo sapiens)

Pain Link Frequency Relevance Heat cINOD 66 99.56 dexamethasone 25 99.36 Dynorphin 1 96.56 Morphine 1 94.72 Kappa opioid receptor 2 91.88 Kinase C 3 84.56 opioid receptor 1 82.12 COX-2 inhibitor 5 77.64 diclofenac 3 75.96 medulla 2 75.20

Disease Link Frequency Relevance Heat Apoptosis 383 99.08 Cancer 805 98.66 Leukemia 22 98.26 Thyroid Neoplasm 1 97.96 Hepatocellular Cancer 84 97.84 Malignant Neoplastic Disease 141 97.08 Breast Cancer 362 96.84 Retinoblastoma 4 96.80 Pancreatic Cancer 4 95.24 Necrosis 6 94.76

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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].

Gene_expression (expression) of p27Kip1 in thyroid associated with thyroid neoplasm

1) Confidence 0.75 Published 2010 Journal Diagn Pathol Section Body Doc Link PMC3017030 Disease Relevance 0.97 Pain Relevance 0

Treatment of HT-29 cells with 5-FU resulted in decreased expressions of p21Cip1 and p27Kip1, and simultaneously in increased expression of CDK2.

Gene_expression (expressions) of p27Kip1 in HT-29

2) Confidence 0.75 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0 Pain Relevance 0

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.

Gene_expression (expressions) of p27Kip1 in HT-29

3) Confidence 0.75 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0.13 Pain Relevance 0

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.

Gene_expression (expressions) of p27Kip1

4) Confidence 0.75 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0 Pain Relevance 0

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.

Gene_expression (expression) of p27kip1

5) Confidence 0.75 Published 2008 Journal PPAR Research Section Body Doc Link PMC2396389 Disease Relevance 0.17 Pain Relevance 0.09

in the transformed foci, and an overexpression of the CKi p27kip1 in

Gene_expression (overexpression) of p27kip1

6) Confidence 0.75 Published 2008 Journal PPAR Research Section Body Doc Link PMC2396389 Disease Relevance 0.56 Pain Relevance 0

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.

Gene_expression (expression) of Kip1

7) Confidence 0.75 Published 2010 Journal J. Neuroimmunol. Section Abstract Doc Link 20163878 Disease Relevance 0.41 Pain Relevance 0.30

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.

Gene_expression (expressions) of kip1 associated with dexamethasone

8) Confidence 0.75 Published 2009 Journal Toxicology Section Abstract Doc Link 19428934 Disease Relevance 0.97 Pain Relevance 1.09

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.

Gene_expression (expressions) of kip1 associated with cinod

9) Confidence 0.75 Published 2009 Journal Toxicology Section Abstract Doc Link 19428934 Disease Relevance 0.78 Pain Relevance 1.03

The p27kip1 expression was up-regulated by indomethacin, celecoxib and dexamethasone in both D1-cells and hBMSCs.

Gene_expression (expression) of p27kip1 associated with dexamethasone

10) Confidence 0.75 Published 2007 Journal Biochem. Pharmacol. Section Abstract Doc Link 17714695 Disease Relevance 0.25 Pain Relevance 0.93

Ectopic overexpression of p21Cip1 or p27KiP1 markedly enhanced the apoptosis induced by sulindac sulfide.

Gene_expression (overexpression) of p27KiP1 associated with apoptosis

11) Confidence 0.75 Published 2001 Journal Anticancer Res. Section Abstract Doc Link 11724286 Disease Relevance 0.81 Pain Relevance 0.13

in the transformed foci, and an overexpression of the CKi p27kip1 in

Gene_expression (overexpression) of p27kip1

12) Confidence 0.65 Published 2008 Journal PPAR Research Section Body Doc Link PMC2396389 Disease Relevance 0.56 Pain Relevance 0

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.

Gene_expression (expression) of p27Kip1 in HT-29

13) Confidence 0.58 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0.06 Pain Relevance 0

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.

Gene_expression (levels) of p27KiP1

14) Confidence 0.58 Published 2001 Journal Anticancer Res. Section Abstract Doc Link 11724286 Disease Relevance 0.80 Pain Relevance 0.15

through increased expression of p21Cip1/Waf1, p27Kip1, and

Gene_expression (expression) of p27Kip1

15) Confidence 0.58 Published 2008 Journal PPAR Research Section Body Doc Link PMC2435221 Disease Relevance 1.29 Pain Relevance 0.04

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).

Gene_expression (expression) of p27Kip1

16) Confidence 0.58 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0.19 Pain Relevance 0

inhibition associated with G1 cell cycle arrest through increasing p27Kip1 protein expression [140, 165–167].

Gene_expression (expression) of p27Kip1

17) Confidence 0.58 Published 2008 Journal PPAR Research Section Body Doc Link PMC2435221 Disease Relevance 1.23 Pain Relevance 0.03

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.

Gene_expression (expressions) of kip1 associated with cinod and apoptosis

18) Confidence 0.58 Published 2009 Journal Toxicology Section Abstract Doc Link 19428934 Disease Relevance 0.82 Pain Relevance 1.03

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].

Gene_expression (expression) of p27Kip1

19) Confidence 0.58 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2072925 Disease Relevance 0.06 Pain Relevance 0.12

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.

Gene_expression (levels) of p27KiP1 associated with leukemia and cancer

20) Confidence 0.58 Published 2001 Journal Anticancer Res. Section Abstract Doc Link 11724286 Disease Relevance 0.76 Pain Relevance 0.11

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