BCL2 expression

Primary EN-DLBCL can involve multiple organs or tissue sites. TP53 , MYD88 , and CD79B are the most common gene mutations. The efficacy of BTKi in patients with positive MCD subtypes at intermediate and high risk is not inferior to that in MCD-negative control patients.

Curcumol may mediate the programmed death of AML cells by inhibiting the PI3K/AKT signaling pathway, affecting the expression of Bcl-2 family proteins, and promoting the activation of core members of Caspase family, so as to play an anti-leukemia role.

A rat epilepsy model was induced in vivo using lithium chloride-pilocarpine...In the recovery experimental group that involved silencing Kv1.1, the beneficial effects of overexpressing ADAR2 were no longer observed (P < 0.05). Our findings confirm that the upregulation of ADAR2 promotes Kv1.1 protein expression, which ultimately reduces neuronal damage in the hippocampus of animals with epilepsy.

In addition, the results showed that isoarborinol acetate and myricitrin compounds have inhibition of alpha-glucosidase and caspase-3. It can be concluded that EEPa is one of the alternative choices to overcome hyperglycemia.

Ub-K48 is strongly linked to the development of AD. p-Tau aggregate in neuronal cells in the hippocampal region of the AD brain and colocalize with Ub-K48, which in turn leads to cellular inflammation and the induction of apoptosis in neuronal cells.

These findings suggest that cataranthine may exert its anticancer effects by reducing oxidative stress and promoting apoptosis, while decrease in miR34 and miR29 as well as increase in Nrf2 and Bcl2 may act as resistance mechanisms in cancer cells. The results highlight the dual potential of cataranthine in regulating cellular responses to oxidative stress and cell death in liver cancer, with dose-dependent modulatory effects.

This study indicated that the potential mechanism of WJD in the prevention and treatment of CRC had the characteristics of the multi-target, multi-path, and multi-system mechanisms, which were mainly related to the regulation of chemokines and the promotion of apoptosis.

No abstract available

P3, N=92, Active, not recruiting, National Cancer Institute (NCI) | N=302 --> 92 | Trial completion date: May 2025 --> Dec 2025 | Trial primary completion date: May 2025 --> Jun 2024

Meanwhile, EBI3 knockdown diminished the phosphorylation levels of both Smad3 and STAT6 and the levels of immune response-relevant cytokines in melanoma cells, while aggravating the macrophage M1 polarization and the expression of cGAS, p-STING and p-IRE1 α in THP-1 monocyte-derived macrophages co-cultured with EBI3-silenced melanoma cells. This study filled the blank on the involvement of EBI3 in melanoma, hinting the possibility of controlling EBI3 as a therapeutic strategy in the management of melanoma.

GANT61 effectively reversed ADR resistance in HL-60/ADR cells by upregulating lysosome activities and downgrading BCL2 expression, providing a new treatment strategy with acceptable toxicity for AML-resistant patients.

Luteolin induces apoptosis and autophagy to inhibit proliferation of A549 cells by increasing ROS production, inhibiting the AKT/mTOR pathway and down-regulating HO-1 protein expression.

MSG induced more severe adverse testicular effects in juvenile rats, while ALO pretreatment was more protective in adult rats. ALO's anti-inflammatory, antioxidant, antiapoptotic, pro-autophagic, antifibrotic, and proliferative actions in the testis suggest its promising potential for combating male reproductive dysfunction.

The produced scFv antibody showed to be functional in a simultaneous blockade of EGFR and HER2, suggesting its potential as a promising candidate for targeted therapy against various EGFR overexpressing tumors.

Overexpressing c-myc, however, may partially counteract this impact. The data show that USP37 may be a potential therapeutic target for DLBCL, and that it may enhance the course of the disease by deubiquitinating c-myc via direct interactions with c-myc.

Treatment with PD98059, SP600125, SB203580, or Bay 11-7082 reversed the effects of TNFRSF12A overexpression on cell proliferation, apoptosis, and proinflammatory cytokine expression. In conclusion, the effects of TNFRSF12A on proliferation, apoptosis, and proinflammatory cytokine expression in THCA cells were regulated by the MAPK and NF-κB pathways.

Furthermore, A‑1331852 suppressed the growth of xenograft tumors derived from 5‑FU‑resistant cells by inducing apoptosis. Overall, the present findings suggested that Bcl‑xL upregulation contributes to 5‑FU resistance of colorectal cancer and targeted inhibition by A‑1331852 may be an effective treatment strategy.

The findings suggest that RES effectively targets the AKT/GSK-3β/NF-kB signaling pathway in glioma cells. Furthermore, RES-loaded albumin nanoparticles significantly enhance therapeutic efficacy by improving cellular penetration, highlighting their potential in advancing GBM treatment strategies.

Results demonstrated that this delivery system can be efficiently and selectively taken up by RGD receptor-positive cells (αvβ3 integrin receptor), further inducing effective target gene knockdown. Overall, this system provided a promising strategy for the targeted delivery of nucleic acid drugs.

This study shows that overexpression of GDF15 reduces OGD/R-induced HT22 cell damage, and ER stress-mediated ferroptosis is included in the regulatory mechanisms. This provides a theoretical basis for GDF15 as a new target for the treatment of cerebral ischemia-reperfusion injury.

Quantitative RT-PCR analysis showed increased Bcl2 gene expression with fold variation level of about 0.086094579. The obtained results emphasized the significance of Nyctanthes arbor-tristis extracts with a suggestion of chemotherapeutic medication to treat various cancers in the future.

Thus, the TYK2/STAT3/Bcl2 axis is a crucial mechanism through which SS18-SSX mediates apoptosis evasion in SS cells. In conclusion, our findings contribute to understanding how SS18-SSX-driven TYK2 expression mediates apoptosis evasion mechanisms and propose targeting TYK2 as a strategy to induce apoptosis in SS.

Activation of the p38 MAPK signaling pathway by anisomycin reduced the therapeutic effects of KAE. The study concluded that KAE could improve the proliferation activity of degenerated NPCs, reduce inflammation levels, and slow the progression of IDD in rats, and the mechanism was likely related to the regulation of the p38 MAPK signaling pathway.

PI3K inhibitor LY294002 intervention could reduce the promoting effect of AU on ribosome biogenesis. The above results suggest that AU can improve the injury of nucleus pulposus cells and ECM degradation, and its mechanism of action is related to its activation of the PI3K/mTOR pathway to promote ribosome biogenesis.

R. roxburghii polysaccharides may inhibit the proliferation of DU145 cells and induce its apoptosis by inhibiting the PI3K/Akt/mTOR pathway and clearing intracellular ROS.

The results showed that the Polygonati Rhizoma aqueous extract alleviated the stomach Yin deficiency in mice, ameliorated gastric mucosal lesions, increased the activities of antioxidant enzymes in the gastric tissue(P<0.05, P<0.01), lowered the levels of pro-inflammatory cytokines in the gastric tissue(P<0.05, P<0.01), down-regulated the expression levels of proteins in the TRAF1/ASK1/JNK pathway(P<0.01) and pro-apoptotic factors in the gastric tissue, and up-regulated the expression of B-cell lymphoma-2(Bcl-2). The results suggested that the Polygonati Rhizoma aqueous extract could alleviate the symptoms of stomach Yin deficiency, such as hunger without desire to eat, thirst, and dry stool, and mitigate the gastric mucosal injury caused by overtaking pungent substances and alcohol by inhibiting the TRAF1/ASK1/JNK pathway to reduce apoptosis and inflammation in the gastric tissue.

In addition, the essential oil inhibited the expression of Iba-1, lowered the levels of TNF-α, IL-1β, and IL-18, and down-regulated the mRNA levels of NLRP3, ASC, and caspase-1 as well as the protein levels of NLRP3, ASC, caspase-1, p-IKKβ(Y188)/IKKβ, p-NF-κB(S536)/NF-κB p65, cleaved caspase-1, and GSDMD-N. The results indicated that the essential oil of Acori Tatarinowii Rhizoma inhibited the NLRP3 inflammasome-mediated pyroptosis of microglia.

rCBV and leakage-corrected rCBV may help differentiate double-expressor from non-double-expressor subtypes in PCNSL.

The expression of B-cell lymphoma 2 (Bcl-2) was significantly increased (p < 0.01, p < 0.05). GA can restore neurological dysfunction and inhibit hippocampal neuronal apoptosis in CI/RI mice, at least partially through inhibition of the JNK/Caspase-3 signaling pathway and regulation of apoptosis signals.

Meanwhile, the released functional nucleic acid G3139 downregulated the expression of Bcl-2, and accelerated the apoptosis of tumor cells. In conclusion, the HTCG@TA demonstrated significant effect in oxidative damage amplification and tumor inhibition both in vitro and in vivo, which has provided a new outlook for the clinical application of chemo-dynamic tumor treatment and synergistic gene therapy with self-delivery nanoplatforms.

Notably, ALA interacted directly with the active site of MMP2 and MMP9. These findings suggest that ALA has the potential to be a promising agent with anti-cancer effects on MG-63 cells, warranting further preclinical investigations.

Our results show that miR-484 may play a roll as an onco-miR in BC. Increased miR-484 and BCL2, and decreased Casp3, in breast tumor tissues suggest that Casp9 expression may increase uncontrolled cell proliferation by suppressing apoptosis in BC cells and may contribute to tumor progression.

High-grade B-cell lymphomas are subclassified based on morphologic and genetic features. There are differences in the nomenclature and definition of these lymphomas in the WHO-5 and ICC classifications. Distinguishing HGBLs from other mature B-cell lymphomas and B-LBL/ALL is critical so that patients receive appropriate treatment.

Furthermore, Rc exerts anti-inflammatory and anti-apoptotic effects through PI3K-AKT and NF-κB signaling pathways. In conclusion, ginsenoside Rc demonstrated significant protective effects against 5-Fu-induced intestinal mucositis via the PI3K-AKT/NF-κB signaling pathway, suggesting its potential as a therapeutic agent for chemotherapy-related mucositis.

SHARPIN was identified as an upregulated anti-apoptotic protein in CRC, and matrine exhibited anticancer effects by downregulating its expression. Thus, matrine appears to be a promising drug for CRC.

Capecitabine enhances miR-29b-3p expression, leading to the downregulation of MMP16, thereby inhibiting proliferation and promoting apoptosis in ovarian cancer cells.

Bcl-2 protein ratios predicting sensitivity to venetoclax in vitro were also able to distinguish patients with shorter time to progression after triplet-based induction therapy and ASCT. This is the first study to assess the expression of the most important Bcl-2 family proteins by a quantitative method in a large set of MM patients according to their cytogenetic abnormalities. We shed light on the impact of these proteins on MM prognosis, which could help to consider the levels of proteins involved in apoptosis in the development of new therapeutic strategies.

The additive effect of CTLA-4 knockdown together with Docetaxel treatment significantly downregulated BCL-2 level and upregulated BAX expression. Our findings support the idea that combining chemotherapy such as Docetaxel with efficient targeted therapy against inhibitory immune checkpoints can be a promising strategy in cancer treatment.

Molecular docking, molecular dynamics (MD) simulations, and MM/GBSA calculations further confirmed the stable binding of voreloxin to both c-Myc and Bcl-2 G4s, primarily driven by π-π stacking and hydrogen bonding interactions. These findings provide valuable insights for the development of G4-targeting drugs for cancer therapy.

Mitoquinone is a mitochondria-targeted antioxidant that can prevent of mitochondrial oxidative damage...Finally, we confirmed that Cur (50 or 100 mg/kg body weight) attenuated DON-induced apoptosis and inflammation by inactivating mtROS. Collectively, these results confirm that DON causes spleen damage by increasing mtROS, and the protective effects of curcumin.

Nerol plays a positive role in alleviating DOX-induced heart failure in rats, possibly by inhibiting cardiomyocyte apoptosis. These findings provide novel evidence and potential targets for developing new cardioprotective drugs.

Findings that robust CLL cycling associates with progressively decreasing BCL2 protein that directly correlates with decreasing venetoclax susceptibility, combined with past findings that these cycling cells have the greatest potential for activation-induced cytosine deaminase (AICDA)-driven mutations, suggest that venetoclax treatment should be accompanied by modalities that selectively target the cycling compartment without eliciting further mutations. The employment of survivin inhibitors might be such an approach.