BCL2 (B-cell CLL/lymphoma 2)

Our study identifies a four-gene cell cycle signature associated with poor LUAD prognosis and demonstrates that astragalin induces apoptosis in LUAD cells. These genes are involved in a PANoptosis-related network, suggesting a potential mechanistic link requiring further validation.

Furthermore, emerging platforms such as RNA interference (RNAi), messenger RNA (mRNA) therapy, and genome editing offer new opportunities to modulate apoptotic signaling. In this review, we summarize the molecular mechanisms of apoptosis in cancer, discuss targeted therapeutic strategies according to their signaling pathways and developmental stages, and outline future directions for apoptosis-based cancer therapy.

Additionally, co-treatment with the autophagy inhibitor chloroquine (CQ) attenuated MA-induced FTH1 downregulation and rescued MA-induced inhibition of cell viability in MDA-MB-231 cells...Bioinformatics analysis identified key hub genes associated with MA-induced autophagy, including tumor protein p53 (TP53), heat shock protein 90 alpha family class a member 1 (HSP90AA1), AKT serine/threonine kinase 1 (AKT1), mTOR, tumor necrosis factor (TNF), interleukin 6 (IL6), epidermal growth factor receptor (EGFR) and BCL2 apoptosis regulator (BCL2), as well as hub genes related to ferroptosis, such as mitogen-activated protein kinase 3 (MAPK3), RELA proto-oncogene (RELA), epidermal growth factor receptor (EGFR), prostaglandin-endoperoxide synthase 2 (PTGS2), SRC proto-oncogene (SRC), interleukin 1 beta (IL1B), interleukin 6 (IL6), and peroxisome proliferator activated receptor gamma (PPARG). In MDA-MB-231 cells, MA triggered autophagy through p53 upregulation and mTOR signaling inhibition, and induced ferroptosis by reprogramming GSH metabolism and activating the NCOA4-mediated ferritinophagy pathway, lead to FTH1 degradation.

This study identifies HSG as a critical tumor suppressor in malignant meningioma that restrains tumor aggressiveness by dampening the Wnt/β-catenin cascade. These novel findings highlight the HSG-Wnt/β-catenin axis as a promising therapeutic target, offering new translational strategies for the management of this highly aggressive intracranial tumor.

SPDEF is specifically downregulated in TNBC, and its high expression is associated with earlier tumor stage and favorable clinical outcomes. SPDEF suppresses TNBC cell proliferation, migration, and invasion while promoting apoptosis through modulation of apoptosis-related protein expression, highlighting its potential as a prognostic biomarker and therapeutic target for TNBC.

These results provide mechanistic information on skeletal metastasis in orthopedic oncology. Dedicated bone metastasis models need to be evaluated.

It also considerably reduced NF-kB p65 and inflammatory markers in comparison with cisplatin alone. Our study demonstrated that rhIGFBP-3 enhanced cisplatin efficacy by promoting apoptosis and attenuating inflammation, highlighting its potential as both a cisplatin adjuvant and a monotherapy in HeLa cells.

Notably, the combination of TQ and PTX was shown to support a greater senotherapeutic effect. Findings indicated that TQ and PTX acted as senotherapeutic agents in 5-FU-induced senescent CRC spheroids and may have potential as adjuvants to enhance CRC therapy.

EA and PSE antioxidants increased hsa-miR-16-5p and hsa-miR-34a-5p expression, induced apoptosis, decreased cell proliferation, and stopped cancer cells in the G1 phase. Therefore, they can be considered promising compounds for helping the treatment of breast cancer.

The effect of GDF11 on chemotherapy sensitivity was investigated in HL60 cells treated with 10 μM daunorubicin (DNR)...In addition, CTSS activated the extracellular signal-regulated kinase 1 and 2 signaling pathway and inhibited endoplasmic reticulum stress in AML cells. In conclusion, GDF11 inhibited the growth and increased chemosensitivity through inhibiting CTSS expression in AML cells, providing potential therapeutic targets for AML treatment.

This study established a potential miRNA-mRNA regulatory network related to tumor biology, providing a comprehensive understanding of the molecular mechanisms and offering new therapeutic targets for liver cancer.

Furthermore, the PI3K/AKT inhibitor LY294002 enhanced the effects of sh-MUC1 on the proliferation, apoptosis, migration, invasion and EMT progress, while the activator SC79 partially restored these effects...To conclude, these findings suggested that MUC1 played an important role in lung cancer progression, potentially through the PI3K/AKT pathway. This positioned MUC1 as a molecule worthy of further investigation for its therapeutic potential.