Co-occurring genomic alterations, particularly in tumour suppressor genes such as TP53 and LKB1 (also known as STK11), have emerged as core determinants of the molecular and clinical heterogeneity of oncogene-driven lung cancer subgroups through their effects on both tumour cell-intrinsic and non-cell-autonomous cancer hallmarks.
TP53 mutations with 0.05-1.0% VAF were more prevalent (p < 0.05) and also enriched for tobacco smoke and age-associated mutation signatures in normal AEC from lung cancer cases compared to non-cancer controls matched for smoking and age.
The present study was aimed to explore the effect of S100A6 on the proliferation, invasion, migration and angiogenesis in lung cancer cell lines with the change of miR-193a expression and P53 acetylation.
These results demonstrate a previously unrecognized relationship between p53 and REV3L in cancer cell metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in lung cancer.
No other statistically significant differences were determined in the plasma p53 protein level between patients diagnosed with lung cancer exposed and not exposed to radon.
The positive expression of p53 and MMP-2 in lung cancer tissues before chemotherapy was 76.25 and 71.25%, respectively, and were reduced to 27.50 and 23.75%, respectively, after chemotherapy.
We went on to study the effect of blocking protein aggregation by emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) and figured that inhibiting p53 protein aggregation can elevate the level of autophagy in A549 lung cancer cell line while there is no significant effect on autophagy in normal non-cancerous HaCaT cells.
Aim of our study was to evaluate the relationship between the polymorphisms of TP53 pathway genes <i>TP53</i>, <i>MDM2</i>, <i>MDM4</i>, the polymorphisms of HPV-associated genes <i>MTHFR</i>, <i>CASP8</i>, <i>CCR5</i>, and HPV infection with survival of LC patients.SNPs were genotyped using PCR-RFLP. qRT-PCR was used to detect, identify, and quantify HPV.
We also identified apoptosis-related genes enriched with ancestor mutations in lung cancers and a relationship between APC hotspot mutations and TP53 mutations in colorectal cancers.
Erastin exposure upregulated and activated p53 and thus, transcriptionally activated its downstream target genes, including p21 and Bax, in lung cancer A549 cells dependent on erastin‑induced ROS.
<b>Methods:</b> The expression of HUWE1 and p53 in lung cancer cells was modulated and the phenotypes were assessed by performing soft agar colony forming assays, cell cycle analysis, BrdU incorporation assays, and xenograft tumor growth assays.