ENO1 (Enolase 1)

Nitrosative stress can promote the malignant biological behavior of breast cancer cells through the glycolytic pathway.

Targeting surface ENO1 with HuL001, a first-in-class humanized antibody, significantly reduced glycolysis, decreased extracellular lactate accumulation, reprogrammed macrophage polarization and inhibited tumor growth and distant metastasis. Moreover, targeting surface ENO1 significantly increased the therapeutic response to radiotherapy and delayed tumor regrowth by increasing antitumoral M1 macrophages and cytotoxic CD8+ T cells infiltration within TME. These results indicated that targeting surface ENO1 remodeled the tumor microenvironment and provided better therapeutic effects to radiotherapy in poorly immunogenic colorectal cancer (CRC) and triple-negative breast cancer (TNBC).

Chidamide combined with ENO1 knockdown enhanced the effect of the inhibitor on promoting apoptosis and cell cycle arrest in PTCL-NOS tumor cells. Taken together, the findings suggest that knockdown of ENO1 activates autophagy and promotes ferroptosis, thereby inhibiting PTCL-NOS cell proliferation.

This study delineates the profound impact of nucleotide metabolic reprogramming on epithelial cell states, immune ecology, and malignant evolution in LUAD. The NMRS provides a robust predictor of prognosis and immunotherapy response across cohorts, while ENO1 emerges as a pivotal metabolic-immune mediator and promising therapeutic target.

In the in vivo orthotopic xenograft osimertinib-resistant models, targeted suppression of the tumor-derived lactate/ENO1 lactylation feedback loop effectively ameliorated resistance to osimertinib. Collectively, our findings provide the basis for targeting lactate/lactate-associated signaling to combat resistance to osimertinib.

In particular, it addresses the most recent advancements in optical and electrochemical biosensors, the analytical capabilities of various biosensors, the challenges, and potential directions for future study in regular clinical analysis. Therefore, this study reviews the latest developments and enhancements (2011-2025) in biosensors for the identification of biomarkers for lung cancer.

This ENO1-mediated aggregation of RRM2 protein increases the synthesis of dNTPs in pancreatic cancer cells, enhancing the resistance of pancreatic cancer to gemcitabine. Our study reveals a role of ENO1 in pancreatic cancer via RRM2-STUB1 axis and provides a scientific basis for the development of new therapeutic strategies targeting ENO1.

RARS1 promotes LIHC progression through oncogenic signaling and immune modulation, serving as a promising prognostic biomarker and therapeutic target. Targeting RARS1 with agents like AH.6809 may offer novel treatment strategies for LIHC.

In conclusion, ENO1 knockdown compromises tumorigenicity and promotes OXPHOS. Combining ENO1 inhibition with oxidative-stress-enhancing treatments, such as chemotherapy or radiotherapy, may further enhance efficacy.

Our study demonstrated that CEACAM6 regulates glycolysis via the ENO1-AKT/mTOR axis. These results offer new evidence about previously unexplored molecular mechanisms driving BCa progression.

This study illuminates PBRM1's tumor suppressor role, highlighting the AKT-mTOR pathway and aerobic glycolysis as potential therapeutic targets in NPC.

The present study confirmed that pachymic acid played an inhibitory role in the proliferation and invasion of colon cancer by intervening in the process of glycolysis. PPARγ was identified as the primary target of pachymic acid in regulating the glucose metabolism in colon cancer.