In conclusion, cisplatin synergistically increased the tumor-killing of CRAd by (1) increasing CRAd transduction via enhanced CAR expression and (2) increasing p53 dependent or independent apoptosis of lung cancer cell lines.
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.
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.
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.
Computational master-regulator search reveals mTOR and PI3K pathways responsible for low sensitivity of NCI-H292 and A427 lung cancer cell lines to cytotoxic action of p53 activator Nutlin-3.
Synergetic and Antagonistic Molecular Effects Mediated by the Feedback Loop of p53 and JNK between Saikosaponin D and SP600125 on Lung Cancer A549 Cells.
<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.
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.
Cytosolic 5'-Nucleotidase II Silencing in a Human Lung Carcinoma Cell Line Opposes Cancer Phenotype with a Concomitant Increase in p53 Phosphorylation.
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.
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.
We conclude that NNK may increase the risk of lung cancer progression and poorer outcomes in patients with p53 mutations by perturbing proper mitotic progression and chromosome integrity.