|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
CDK2 and its regulatory subunits are deregulated in many human cancers and there is emerging evidence suggesting CDK2 inhibition elicits antitumor activity in a subset of tumors with defined genetic features.
|
31839441 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The results showed that GY-1 showed good anti-liver cancer activity with the IC<sub>50</sub> of 84.7 μmol/L in vitro, inhibited tumor growth in vivo with dose-dependent, and GY-1 could arrest the growth of hepatoma cells in the S phase and induced apoptosis in hepatoma cells, down-regulated the expression of C-myc, CDK2 and CyclinE, and up-regulate p53.
|
31797046 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
CDK2 destabilizes tumor suppressor C/EBPα expression through ubiquitin-mediated proteasome degradation in acute myeloid leukemia.
|
31692040 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Interestingly, we discovered that p-CDK2 protein was expressed in both cytoplasmic and nucleus in salivary ACC tissues, which was higher than that in normal salivary tissues, indicating that agents targeting CDK2 may be potential therapeutic strategies against this type of tumor.
|
31529315 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
CDK2 mRNA expression was associated with tumor diameter, TNM stage, lymph node metastasis, and serum alpha-fetoprotein levels (P<0.05).
|
30947664 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This positive effect on tumor growth involves activation of c-myc and cyclin E1/CDK2 and their effect on cell cycle distribution.
|
30675171 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In this large panel, high expression of both CDK2 and SEPT2 significantly correlates with tumor differentiation and microvascular invasion, which is an independent prognostic factor in HCC patients.
|
30444001 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
CDK2 activity is largely dispensable for normal development, but it is critically associated with tumor growth in multiple cancer types.
|
30543440 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We uncovered a molecular dependence on the CCNE-CDK2 cell cycle complex that renders CIC-DUX4-expressing tumors sensitive to inhibition of the CCNE-CDK2 complex, suggesting a therapeutic strategy for CIC-DUX4-expressing tumors.
|
31329165 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Mechanism explorations showed that silencing CDK2 increased expression of the SIRT5 tumor suppressor.
|
29896817 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we show that miR-3140, which was identified as a novel tumor suppressive miRNA by function-based screening of a library containing 1090 miRNA mimics, directly suppressed BRD4 by binding to its coding sequence (CDS). miR-3140 concurrently downregulated BRD3 by bind to its CDS as well as CDK2 and EGFR by binding to their 3' untranslated regions. miR-3140 inhibited tumor cell growth in vitro in various cancer cell lines, including EGFR tyrosine kinase inhibitor-resistant cells.
|
29540837 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Such drug-mediated cyclin E induction in TNBC cells and PDX models sensitizes them to AZD1775 in a sequential treatment combination strategy.<b>Conclusions:</b> Cyclin E is a potential biomarker of response (i) for AZD1775 as monotherapy in cyclin E-high TNBC tumors and (ii) for sequential combination therapy with CDK2 inhibitor or carboplatin followed by AZD1775 in cyclin E-low TNBC tumors.
|
30181387 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
LMW-E expression overcame cell-cycle inhibition by AIs in a CDK2/Rb-dependent manner, and inhibition of CDK2 by dinaciclib reversed LMW-E-mediated resistance, whereas treatment with palbociclib, a CDK4/6 inhibitor, did not.<b>Conclusions:</b> Collectively, these findings suggest that cell-cycle deregulation by LMW-E mediates resistance to AIs and a combination of CDK2 inhibitors and AIs may be an effective treatment in patients with HR-positive tumors that express LMW-E. <i></i>.
|
28947566 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, inhibition of pERK both reduced levels of CDK2 and prevented EMT independent of exogenous TGFβ, consistent with most observations identifying pERK as a tumor promoter.
|
28368414 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increased CDK2 activity decreases risk in colon cancer, but elevates poor outcome two- to fivefold in specific tumors, including low grade glioma, kidney, thyroid, adrenocortical and prostate cancer.
|
27819669 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Structural prediction of the interaction of the tumor suppressor p27<sup>KIP1</sup> with cyclin A/CDK2 identifies a novel catalytically relevant determinant.
|
28056778 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our findings provide a rationale for clinical use of Bcl-2 family inhibitors in combination with CDK2 inhibitors for treatment of Mcl-1-dependent colorectal tumours associated with expression of Bcl-2, Bcl-XL and Bcl-w proteins.
|
29372687 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, real-time PCR and Western blot analyses were conducted to examine expression levels of cell cycle regulatory proteins cyclin A and cyclin-dependent kinase 2 (CDK2), as well as their mediators tumor suppressor genes p53 and p16.
|
27098147 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The activation of CHK1/CDC25A/CDK2 pathway was also demonstrated in Mus81-inhibited HepG2 cells and xenograft mouse tumors under EPI treatment.
|
26714930 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data show that CDK2 inhibition may be useful for cancer prevention in premalignant hyperproliferative lesions, as well as established tumors.
|
25149358 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Pituitaries of Men1(+/-); Cdk4(-/-) mice showed no signs of loss of heterozygosity (LOH) in the Men1 locus, whereas tumors in Men1(+/-) mice and Men1(+/-); Cdk2(-/-) mice exhibited LOH.
|
24531709 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
A group of the altered miRNAs were identified by miRNA target prediction tools for regulation of the INK4/CDKN2 family tumor suppressor genes. miRNA-141 was experimentally validated for INK4A 3'-UTR target binding in the CMT cell lines providing an essential mechanism for the post-transcriptional regulation of the INK4A tumor suppressor gene in CMT models.
|
26095675 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We observed that TQ inhibited tumor cell growth in vitro, where treatment with TQ arrested the cell cycle in G1 by upregulating p21 and downregulating cyclinD1 and CDK2 expression; moreover, TQ induced apoptosis by decreasing expression of Bcl-2 and increasing expression of Bax.
|
26416455 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In the validation cohort, CDK2-specific activity (P = 0.0368) was identified as an independent prognostic factor for tumor recurrences with tumor location (P = 0.0442).
|
25707496 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Embelin-treated mice showed significant inhibition in tumor growth which was associated with reduced expression of markers of cell proliferation (Ki67, PCNA and Bcl-2) and cell cycle (cyclin D1, CDK2, and CDK6), and induction of apoptosis (activation of caspase-3 and cleavage of PARP, and increased expression of Bax).
|
24694877 |
2014 |