Treatment with HPE or its polyphenol components inhibited the UVB-induced damage by removing an excess of reactive oxygen species (ROS), reducing DNA damage and p53 activation, regulating the protein expression of B-cell lymphoma 2 family members toward antiapoptotic ratios, and reducing caspase activation.
We identified 122 patients diagnosed as having large B-cell lymphoma (44, MYC-negative; 29, MYC-EC; 23, MYC rearrangement; 22, MYC and BCL2 rearrangements; 4, MYC, BCL2, and BCL6 rearrangements). p53 expression significantly correlated with DLBCL with abnormal MYC status (MYC-EC, MYC rearrangement, and MYC overexpression), but adverse p53 prognostic effect was only seen with MYC-rearranged lymphoma.
Compared with those in the control group, the apoptosis rate of T24 cells was remarkably increased after treatment with different doses of puerarin or EX527, and the expression level of apoptosis-related protein Bcl-2-associated X protein (Bax) was also significantly increased, but the expression level of B-cell lymphoma 2 (Bcl-2) was decreased, and both the protein and mRNA expression levels of SIRT1 and p53 also significantly declined.
However, the mRNA expression level of antiapoptotic B-cell lymphoma-2 was markedly decreased by <i>P. undulata</i> treatment.Moreover, <i>P. undulata</i> increased the protein expression of proapoptotic p53 and caspase 3/9 with reducing B-cell lymphoma-2 protein expression level.Thus, <i>P. undulata</i> induced apoptosis in the HepG2 cells by overexpression of miR-34a which regulates p53/B-cell lymphoma-2/caspases signaling pathway.
PTEN, WWP2, p53 and c-Myc expressions might be served as biomarkers for identification of B cell lymphomas from RFH as well as distinguishing different B cell lymphoma subtypes.
Furthermore, histone-associated DNA fragments levels were measured using a cell-death detection ELISA; BAX (bcl-2-like protein 4), BCL2 (B-cell lymphoma 2), caspases (-3, -8, and -9), p53 mRNA, and protein expression were assessed using real time PCR and immunoblotting.
Our studies showed that the recombinant lamprey PDCD5 protein and transfection of the L-PDCD5 gene induced cell apoptosis, upregulated the expression of the associated X protein (BAX) and TP53 and downregulated the expression of B cell lymphoma 2 (BCL-2) independent of Caspase 3.
GSE + GSK also caused significant cell cycle arrest at the G1 phase, activation of caspase-3, increase in p53 and Bax expression, and decrease in B-cell lymphoma 2 expression and B-cell lymphoma 2:Bax ratio in tumor cells.
Meanwhile, changes in p53 and related proteins were observed including the upregulation of p53, the phosphorylation of p53, p21, B-cell lymphoma-2-associated X protein, and NOXA; and the downregulation of B-cell lymphoma 2.
KGN cells were also transfected with a BANCR expression vector, after which, cell proliferation, apoptosis and the expression levels of pro‑apoptotic B‑cell lymphoma 2‑associated X protein (Bax) and p53 were detected by Cell Counting kit‑8 assay, MTT assay and western blotting, respectively.
Mechanically, DLN did not function by reducing miR‑21 expression, whereas DLN and miR‑21 inhibitor downregulated B‑cell lymphoma-2 (BCL‑2) expression, and facilitated BCL‑2‑associated X protein (Bax) and P53 expression in melanoma cells.
It was also demonstrated that silencing SERPINC1 upregulated the expression of B‑cell lymphoma-2 (Bcl‑2)‑associated X protein and p53 mRNA and protein, and downregulated that of Bcl‑2, survivin and cyclin D1.
For the immunohistochemical analysis, the following antibodies (markers) were used: Ki67, p53 and B-cell lymphoma 2 (Bcl-2), E-cadherin, and vascular endothelial growth factor (VEGF).
The roles of caspase‑3, poly (ADP‑ribose) polymerase (PARP), p53 and B-cell lymphoma (Bcl)‑2/Bcl‑2 associated X, apoptosis regulator (Bax) proteins in the apoptosis of human K562 cells were further examined through western blot analysis.
The DEGs were as follows: Phosphatidylinositol‑dependent kinase 1 (PDK1), a key gene upstream of protein kinase B (AKT); angiopoietin 2, a B‑cell lymphoma 2 (Bcl‑2)‑inhibited gene; transcription factor 4, glutathione S‑transferase P91 and ubiquitin‑specific protease 33, mitogen‑activated protein kinase (MAPK)‑related genes; oxidative stress induced growth inhibitor 1, related to the P53 pathway; Bcl‑2, P53, ERK (MAPK1/3), c‑Jun N‑terminal kinase (MAPK8/9), and P38 (MAPK14), all of which are key genes involved in the AKT signaling pathway.
Mechanistically, the apoptosis-related protein, B-cell lymphoma-2 (Bcl-2), was downregulated in KIFC1 small interfering RNA-treated groups, whereas thee levels of Bcl-2-associated X protein and p53 were upregulated.
The study further demonstrated that combined treatment significantly decreased HEC apoptosis through the upregulation of B-cell lymphoma 2 (Bcl-2) and P53 expression levels, as well as downregulation of Bcl-2-associated X protein and caspase-3 levels.
Alteration to down-stream signaling of p53 including activation of pro-apoptosis protein (Bcl-2-associated X protein; Bax), reduction of anti-apoptosis (B cell lymphoma 2; Bcl-2 and myeloid cell leukemia 1; Mcl-1) and suppression on protein kinase B (Akt) survival pathway were notified in TDB-treated lung cancer cells.
Cu complexes exerted chemotherapeutic effects via activating p53 and inducing production of reactive oxygen species to regulate expression of the B-cell lymphoma-2 family of proteins, causing a change in the mitochondrial membrane potential and release of cytochrome c to form a dimer with apoptosis protease activating factor-1, resulting in activation of caspase-9/3 to induce apoptosis.
We found that Evo significantly induced cell cycle arrest at the G2/M phase, upregulated P53 and Bcl-2 associated X proteins (Bax) proteins, and downregulated B-cell lymphoma-2 (Bcl-2), cyclinB1, and cdc2 proteins in HCC cells.
Damnacanthal treatment increased caspase-3/8 and 9 activity, and promoted B-cell lymphoma 2-associated X protein, tumor protein p53 (p53) and p21 protein expression levels in melanoma cells.
Furthermore, the expression levels of cell apoptosis-associated proteins were determined in the current study, and the data demonstrated that the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and phosphorylated extracellular signal-regulated kinase expression were significantly reduced, while the p53 and caspase 3 levels were notably increased in YAP gene-inhibited ECA-109 cells.
Functional yeast-based assay was performed to analyze p53 mutational status. p53β transfected 786-O and CAKi-1 cells were cultured to examine expressions of B-cell lymphoma 2-associated X protein (bax) and caspase-3, and ratios of apoptosis.