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).

These findings indicate that circNR3C1 promotes ALL cell proliferation and inhibits apoptosis by interacting with MSI2 to stabilize ENO1 mRNA, leading to upregulation of ENO1 and RPS3. The circNR3C1/MSI2/ENO1/RPS3 axis represents a novel regulatory pathway contributing to ALL progression and offers potential therapeutic targets for treatment.

P1/2, N=21, Enrolling by invitation, HuniLife Biotechnology, Inc.

In summary, we demonstrated that LncPRESS1 facilitated BRCA progression and cisplatin resistance via activation of ENO1-mediated glycolysis. Combination of ENO1 inhibitor and cisplatin was a promising therapeutic stragtegy for BRCA patients with overexpression of LncPRESS1.

P1, N=24, Completed, HuniLife Biotechnology, Inc. | Recruiting --> Completed

In summary, this study demonstrates that ICAT, by regulating the c-Myc-ENO1 axis, mediates the interaction between tumor cells and macrophages, thereby reshaping the TME and promoting the migration, invasion, and glycolysis of CC. These findings demonstrate that ICAT represents a potential therapeutic target for the treatment of CC.

Targeting SLKv hindered glycolysis and tumorigenesis. These findings establish SLKv as a critical promoter of glycolysis and a metabolic target for cancer therapy.

The tRF-17-877S6V2/ENO1 axis was demonstrated to modulate CRC cell radiation response through regulation of DNA damage repair and cellular survival pathways. This study characterizes the tRF-17-877S6V2/ENO1 regulatory axis as a novel mechanism in CRC radioresistance and a potential therapeutic target for improving radiation outcomes.

We then explored the effects of the selective PIM1 inhibitor TP-3654 on fibrosis...Downregulation of PIM1 expression in fibroblasts using drugs or siRNA leads to decreased ENO1 expression, concurrent with AKT phosphorylation reduction and suppressor of mothers against decapentaplegic (Smad)2/3 dephosphorylation within the TGF-β classical pathway. In summary, PIM1 might be an important target gene for future skeletal muscle atrophy treatments.

Combination analysis indicated that the s-ENO1-Ab-positive (+)/carcinoembryonic antigen (CEA)-negative (-) group demonstrated a significantly improved prognosis compared with that of the s-ENO1-Ab(-)/CEA(+) group (P<0.01), while a comparison of the s-SSNA1-Ab(+)/CEA(-) group with the s-SSNA1-Ab(-)/CEA(+) group also demonstrated a significant improvement in prognosis (P<0.01). Thus, s-ENO1-Abs and s-SSNA-Abs may be useful biomarkers for predicting gastric cancer prognosis, providing future research directions for novel approaches to target and treat gastric cancer.

Nevertheless, repression of EMT and Wnt pathway progression by Silibinin was perceived from the gene expression studies. Overall, the current study highlights the tweaking of intricate signaling crosstalk between glycolysis and the Wnt pathway in TNBC cells through inhibiting ENO1 and GLUT4.

ENO1 is a tumor biomarker and represents a promising target for tumor therapy. This review summarizes recent advances from 2020 to 2024 in understanding the relationship between ENO1 and tumors and explores the latest targeted therapeutic strategies involving ENO1.