More important, we discovered that VCAN-AS1 expression was negatively correlated with wild-type p53 levels in GC tissues and that p53 was negatively modulated by VCAN-AS1 in GC cells.
Furthermore, LKB1 expression in GC was inversely associated with p53 (<i>r</i>=-0.181, <i>P</i>=0.027) and survivin expression (<i>r</i>=-0.198, <i>P</i>=0.015).
Our results demonstrated that PURPL RNA level in GC was significantly related to tumor size and histopathological grade. p53 expression at both protein and mRNA levels were significantly decreased in GC tissues compared to adjacent control samples.
The molecular subtypes combining the CIMP and TP53 hot spot mutation status provide distinct clinicopathological features and prognostic impacts in GC.
TP53 mutations were highly recurrent (11/14; 79%) in MLH1-positive miGCs and were detected even in two microscopic lesions measuring 1 and 3 mm, respectively.
ENE was present in 36% of patients.EBV-positive carcinoma was evident in 5.8%, and p53 aberrant (chromosomal instable) tumors in 22.2%, a gastric cancer with deficient mismatch-repair status in 9%, and MSS/p53neg/EBVneg tumors were seen in 63% of patients.
XPO1 inhibition induced cell cycle arrest through p53 activation, but the mechanisms of p53 activation differed among the different types of cancer cells. p53 activation depended on the formation of promyelocytic leukemia (PML) nuclear bodies in gastric cancer and liver cancer cells.
Current evidence highlights the key function of SOX9 in GC and postulates it as a prognostic factor, novel biomarker for patient stratification and a promising target. gCSCs are critical targets for GC eradication and SOX9 is a regulator of gCSCs; hence, the inhibition of SOX9 is a potential therapeutic strategy for GC, particularly for the MSS/TP53+ subgroup of patients in whom SOX9 expression correlates with poor outcome.
In this study, we evaluated prevalence of Her3 in gastric cancer, in a Saudi cohort of cases, along with its association with prognostic markers p53 and Ki-67.
Solamargine increased the expression of long noncoding RNA (lnc) p53 induced transcript and lnc nuclear paraspeckle assembly transcript 1 (NEAT1)_2 (P<0.01) in GC by reducing the phosphorylation of extracellular signal‑regulated kinase (Erk)1/2 mitogen‑activated protein kinase (MAPK).
TP53 was shown to be upregulated in the H. pylori-positive group in both TCGA database and RNA sequencing data, which also showed higher expression in the GC tissues than in adjacent normal tissues (P < 0.05).