We demonstrated that CCDC106 knockdown enhanced apoptosis by stabilizing p53 and suppressed cell viability, colony formation, migration and invasion in cervical cancer HeLa and breast cancer MCF7 cells with wild-type p53 (wtp53), whereas CCDC106 overexpression exerted the opposite effects in normal breast epithelial HBL100 and cervical cancer SiHa cells with wtp53.
Statistically, no significant correlation between p53 overexpression and depth of invasion, lymph node involvement, or grade of tumor differentiation was detected.
Because the single knockout of TP53 generates thymic lymphoma, FIR⁺/⁻TP53⁻/⁻ generated T-cell type acute lymphocytic/lymphoblastic leukemia (T-ALL) with increased organ or bone marrow invasion with poor prognosis.
Loss of p53 protein function influences not only cell cycle checkpoint controls and apoptosis, but also the regulation of other important stages of metastatic progression, such as cell migration and tissue invasion.
We describe strategies to: i) target EGFR, its ligand-independent variant EGFRvIII, and PDGFR on the cell surface, ii) inhibit constitutively activate RAS/MAPK and PI3K/Akt signaling pathways, iii) target TP53 mutant tumors, and iv) block GBM angiogenesis and invasion.
Cell viability and proliferation, cell cycle analysis, cell migration and invasion and protein expression and phosphorylation status of Akt and p53 upon SFN treatment were determined.
In addition, CKMT2, miR-93b-5p, miR-29b-3p were found to be positively/negatively correlated with TP53, EGFR, and MMP members mediated OS development, including angiogenesis, migration and invasion.
Therefore, p53 mutation may precede invasion in esophageal carcinogenesis, and multifocal esophageal neoplasms may arise from independent clones of transformed cells.
An expression of Ki67 in 20% or more of tumor cell nuclei, on the other hand, correlated significantly with histological grade 3 (p < 0.0001), nuclear grade 3 (p < 0.0001), absence of ER (p < 0.0001) and of PR (p < 0.0001), c-erb-B2 expression (p < 0.0001), p53 expression (p < 0.0001) and tumor size (p = 0.0005), but not with nodal invasion.
Specific p53 nuclear staining was detected in primary tumor from 50 patients (46.7%). p53 nuclear overexpression was not significantly correlated with patients' sex, age, tumor location, differentiation, T stage, N stage, and lymphatic and/or vascular vessel invasion.
The paraffin-embedded tumor specimens were evaluated for tumor differentiation, tumor thickness and tumor invasion, microvessel density, and p53 expression.
Wip1 may involved in the biological processes of nasopharyngeal cancer cell proliferation, apoptosis, and migration and invasion by regulation P53 and P16 protein expression.
TP53 mutations were associated with extramural venous invasion on baseline MRI (78% vs. 65%, p = 0.04), poor pathological tumour regression (23% vs. 36%, p = 0.05) and a trend toward a worse 5-year progression-free survival (PFS; 60% vs. 74%, HR 1.59, p = 0.06).
We demonstrate that mutant p53 manipulates the gene expression pattern of cancer cells to facilitate invasion through the release of a pro-invasive secretome into the tumor microenvironment.
Kaplan-Meier survival curves and Cox regression analysis were used to determine predictors for overall survival rate. p53 expression status (positive or negative) was significantly different between patient groups when categorized by age distribution, disease course, tumor location, maximum tumor diameter, depth of tumor invasion, Dukes' stage, distant metastasis and lymph node (LN) metastasis (P<0.05).
Esophageal cells overexpressing epidermal growth factor receptor (EGFR) and TP53 mutation can invade into the extracellular matrix when grown in 3D-organotypic cultures (OTC) and mimic early invasion in esophageal squamous cell carcinoma (ESCC).
Wip1 may involved in the biological processes of kidney cancer cell proliferation, apoptosis, and migration and invasion by regulation P53 and P16 protein expression.
Here we identified distinct novel non-canonical transcriptome networks involved in cell proliferation, EMT, chemoresistance and invasion that arise following abrogation of p53 function in vitro and development of CIN in vivo.