Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We previously discovered that deletion of cell cycle inhibitors p16<sup>Ink4a</sup> (p16) or p18<sup>Ink4c</sup> (p18) is required for development of Brca1-deficient basal-like mammary tumors, and that mice lacking p18 develop luminal-type mammary tumors.
|
29996906 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In contrast, miR-188-5p exerted its tumor promoter roles through targeting UBE2I with a subsequent activation of the CCND1-RNASEL-CDKN1A-MDM2 axis.
|
29467540 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Xenograft tumour growth assays demonstrated the P18 peptide suppressed angiogenesis of HCC in vivo.
|
28627623 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
However, the underlying mechanism by which Ubc9 promotes tumor progress and influences the susceptibility to antitumor agents remains elusive.
|
27878232 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We found that relative to adjacent normal tissues, UBC9 was markedly overexpressed in HCC, which closely correlated with tumor size, tumor microsatellite formation, and tumor encapsulation.
|
28572537 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RNAi depletion of the SUMO E2 ligase Ubc9 suppresses 3D growth of KRAS mutant colorectal cancer cells in vitro and attenuates tumor growth in vivo.
|
25805818 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To investigate the importance of the SUMO pathway in the context of cancer cell proliferation and tumor growth, we applied lentivirus-based short hairpin RNAs (shRNA) to knockdown SUMO pathway genes in human cancer cells. shRNAs for SAE2 and UBC9 reduced SUMO conjugation activity and inhibited proliferation of human cancer cells.
|
25860128 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Next, we hypothesized that HULC might function through regulating a tumor suppressor gene p18 located near HULC in the same chromosome.
|
22685290 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, binding of BRCA1 proteins to nuclear chaperone Ubc9 provides a novel mechanism for nuclear import and control of tumor growth.
|
21344391 |
2011 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The levels of Ubc9 were higher in all tumor cell lines, compared to the normal cells, and this probably contributes to over-accumulation of nIGF-1R.
|
21147068 |
2011 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In this study, we genotyped SUMO1 and UBC9 polymorphisms in 147 non-small-cell lung cancer (NSCLC) treated with irinotecan chemotherapy to investigate the association between genotypes and tumor response rate.
|
19859084 |
2010 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The study revealed associations of four UBC9 polymorphisms with risk of grade 1 tumors.
|
19760037 |
2010 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We have earlier reported that Ubc9 promotes tumor growth in the xenograft mouse model using breast cancer cell line MCF-7 in part through regulation of Bcl-2 expression.
|
20023705 |
2010 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, an examination of eight pairs of matched breast tumor specimens by Western blot analysis revealed that, on average, the level of Ubc9 is 5.7-fold higher in tumor than in the matched normal breast tissue.
|
19223510 |
2009 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Recent reports indicate that Ubc9, the single SUMO E2 enzyme catalyzing the conjugation of SUMO to target proteins, is overexpressed in certain tumors, such as lung adenocarcinoma, ovarian carcinoma and melanoma, suggestive of its clinic significance.
|
16758298 |
2006 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Inoculating these cells as xenografts in mice revealed that tumors expressing Ubc9-WT grew better than the vector control, while tumors expressing Ubc9-DN exhibited reduced growth.
|
15735760 |
2005 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To examine the function of p18 as a putative tumor suppressor in myeloma cells, a zinc-inducible p18 construct was stably transfected into KMS12, a MM cell line with biallelic p18 and monoallelic p16 deletions as well as cyclin D1 overexpression.
|
11840272 |
2002 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
HLF, which was deficient in the protein product of the retinoblastoma tumor-suppressor gene (pRb), responded most profoundly to troglitazone, showing an increased expression in not only p21, but also in p27 and in p18.
|
11343236 |
2001 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
By virtue of its structural and functional similarities with the p16 gene, p18 has been implicated as a tumour suppressor gene in a variety of cancers.
|
10736068 |
2000 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The cyclin-dependent kinase inhibitors known as p15, p16, p18 and p19 have been suggested as candidates for tumor suppressor genes.
|
9639410 |
1998 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The CDKN2C gene coding for the cyclin-dependent kinase inhibitor p18 is localized on 1p32, a region frequently involved in chromosomal changes in melanomas and other tumors.
|
9724087 |
1998 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The p15(INK4B), p16(INK4) and p18 genes are members of the gene family coding for inhibitors of cyclin-dependent kinases 4 and 6. p15(INK4B) and p16(INK4) are located at 9p21, a chromosomal region frequently deleted in many human neoplasms.
|
8631583 |
1996 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our results suggest that p18 inactivation by point mutations may contribute to deregulated growth control in certain cell lines and/or tumors.
|
8840966 |
1996 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
With the exception of one breast cancer cell line, no deletions or mutations were found in the p18 gene in either cultured cell lines or primary tumors.
|
8570224 |
1996 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results do not support a role for p18 in the pathogenesis of the lymphoid neoplasms studied.
|
8637248 |
1996 |