In the OBX + GEM group, BxPC‑3 cell activity decreased significantly, cell migration and invasion decreased significantly, the expression of vimentin was significantly reduced and the expression of E‑cadherin and p53 further increased.
Using the SKBR3 breast cancer and p53-null H1299 lung cancer cells stably expressing the R175Hp53 mutant protein, we demonstrated that GON triggers the appearance of a wild-type-like p53 protein by using conformation-specific antibodies, immunoprecipitation, DNA-binding assays and target gene expression. p53 restoration was associated with a G2/M arrest, senescence, reduced cell migration, invasion and increased cell death.
Deregulated p53 pathway components have been implicated in GBM cell invasion, migration, proliferation, evasion of apoptosis, and cancer cell stemness.
The overexpression of PinX1 in CD133+ CSCs significantly decreased hTERT (P < 0.001), inhibited proliferation, migration, and invasion, induced apoptosis, and significantly decreased c-Myc mRNA levels (P < 0.001), while it increased TRF1, Mad1, and p53 mRNA levels (all P < 0.001).
Further, LHPP over-expression reduced the cell proliferation, migration and invasion, associated with the change of p53 and metastasis signaling pathways.
A multivariate Cox analysis revealed that therapy and high p53 expression and venous invasion were independent predictors of unfavorable prognosis in overall survival (<i>p</i>=0.039, <i>p</i>=0.004, and <i>p</i>=0.023, respectively).
TP53 is associated with human cancer by mutations that lead to a loss of wild-type p53 function as well as mutations that confer alternate oncogenic functions that enable them to promote invasion, metastasis, proliferation, and cell survival.
Furthermore, the examination of cell proliferation, apoptosis, and invasion revealed that both miR-15b and p53 inhibited the proliferation and invasion, but promoted the apoptosis, of glioma cells.
Activating PI-3 kinase and Ras pathway mutations were early events, and inactivating mutations in tumor suppressors including RB1, CDKN2A, and TP53 were associated with invasion in individual cases.
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.
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).
The two groups were well balanced in gender, age, body mass index, American Society of Anesthesiologists scores, and number of lymph nodes harvested. p53 positive was associated with carcinoembryonic antigen ≥5 ng/mL ( p = 0.036), gross type ( p = 0.037), degree of tumor differentiation ( p = 0.026), pathological tumor stage ( p = 0.019), pathological node stage ( p = 0.004), pathological tumor-node-metastasis stage ( p = 0.017), nerve invasion ( p = 0.008), and vessel invasion ( p = 0.018).
Although p53 was distributed to the cytoplasm in Apc<sup>Δ716</sup> Trp53<sup>+/R270H</sup> heterozygous tumors, it accumulated in the nuclei at the invasion front, suggesting a regulation mechanism for p53 localization by the microenvironment.
In PBK/TOPK-overexpressing GC cells, knockdown of PBK/TOPK inhibited the cell proliferation through the p53 activation in a TP53 mutation-dependent manner and inhibited the migration/invasion through the PTEN upregulation in a TP53 mutation-independent manner.
Novel phenylenediamine bridged mixed ligands dimetallic square planner Pt(II) complex inhibits MMPs expression via p53 and caspase-dependent signaling and suppress cancer metastasis and invasion.
Here, we investigated the role of mutant p53 in cell migration and invasion as well as its underlying molecular mechanisms in human ovarian cancer cells.