PROM2 (Prominin 2)

The cuproptosis/ferroptosis-related genes-based signature serves as a reliable prognostic tool, reflecting immune landscape remodeling and genomic instability in BRCA. These findings provide insights into subtype-specific therapeutic vulnerabilities and suggest potential strategies for targeting cuproptosis/ferroptosis pathways in precision oncology.

However, critical challenges persist in understanding the molecular interaction networks underlying miRNA dynamics, spatiotemporal heterogeneity of non-canonical pathways, and clinical translation mechanisms. Future investigations should integrate multi-omics data with systems biology approaches to decipher core molecular targets within miRNA regulatory networks, thereby advancing the optimization of precision diagnosis and treatment systems for bladder cancer.

Functional assays following siRNA-mediated knockdown of TMED10 and PROM2 in A2780 and OVCAR3 cells revealed significant reductions in proliferation, colony formation, and migration. These findings highlight SNRPA1, LSM4, TMED10, and PROM2 as potential diagnostic markers and therapeutic targets in OC, warranting further investigation for clinical translation.

Our results suggest that PROM2 is an oncogenic gene that supports BC progression by enhancing glycolysis and inhibiting ferroptosis via AKT/mTOR signaling. Therefore, PROM2 may be a potential therapeutic target for BC treatment.

To optimize risk stratification and survival prediction for CD58mut patients, biological mechanism of the poorer prognosis in high-risk group may be related to the greater abundance of immunosuppressive cells, especially M2 macrophages. Our results indicated that CD58mut could serve as a novel prognostic factor for DLBCL patients, and further exploration of personalized treatment strategies for high-risk DLBCL patients based on the risk score model is needed.

These findings delineate a CRM1-PROM2 signaling axis that governs ferroptosis sensitivity in GC, wherein CRM1-mediated nuclear export of PROM2 during ferroptosis represents a critical regulatory node. Targeting this axis may offer novel diagnostic and therapeutic strategies for GC and other malignancies.

Our study provided a comprehensive landscape of the cancer survival difference and related PCD-TME interaction axis and highlighted that high-apoptosis/pyroptosis states caused favorable prognosis, underlying mechanisms closely related with the TME where anti-tumor immunity would be beneficial for patient prognosis. These findings highlighted the model's potential for risk stratification in BC.

The secondary metabolites from Pseudomonas frederiksbergensis exhibit significant anti-tumor effects and highlight their potential molecular mechanisms in breast cancer regulation. This study provides insights into the therapeutic potential of these metabolites and lays the groundwork for future preclinical and in vivo investigations.

Importantly, rescue experiments elucidated that PI3K/AKT pathway activation could reverse the inhibitory effect of PROM2 silencing on the proliferation, migration, and invasion of NCI-H520 and A549 cells. This study verified that PROM2 knockdown inhibits the growth, migration, and invasion of NSCLC by repressing the PI3K/AKT pathway.

This study identifies the HOXC11/PROM2/PI3K/AKT axis as a novel regulatory mechanism underlying ART-induced ferroptosis in ovarian cancer. Targeting the HOXC11/PROM2 axis may represent a promising therapeutic strategy for enhancing ferroptosis, offering new insights for the treatment of ovarian cancer.

ATF1 could promote ferroptosis resistance in lung cancer through enhancing mRNA stability of PROM2. Thus, our work might shed novel insights on discovering therapeutic strategy for lung cancer.

Attention is paid to certain pathways, such as the FSP1-independent regulation of glutathione, involvement of cholesterol, and the prominin 2-MVB/exosome-ferritin pathway. Ferroptosis plays a key role in resistance to tumor therapy.