FBP1 (Fructose-Bisphosphatase 1)

Thus, prolonged ATF6α activation drives ER stress, leading to glycolysis-dependent immunosuppression in liver cancer and sensitizing to ICB. Our findings suggest that persistently activated ATF6α is a tumour driver, a potential stratification marker for ICB response and a therapeutic target for HCC.

CHE might suppress M2 polarization and tumour progression by targeting FBP1. These findings highlight its potential as a therapeutic agent in immunotherapy and BC treatment.

FBP1 (K51) K48-linked polyubiquitination mediated protein degradation can also promote cancer progression, similarly to the O-GlcNAcylation of FBP1-S47. Our data uncover a mechanism whereby FBP1 can be regulated by a protein O-GlcNAcylation-polyubiquitination axis, paving the way to cancer cell metabolic reprogramming.

However, up to now few reviews have systematically summarized the important functional mechanisms of FBP1 in tumorigenesis and the small molecule compounds that restore FBP1 expression. Therefore, this article addresses the question "How does FBP1 contribute to cancer progression, and can targeting FBP1 be a potential therapeutic approach?" by summarizing the effects of FBP1 on cancer development and progression as well as its mediated drug resistance and the future clinical applications of potential small molecule modulators targeting FBP1.

Future therapeutic strategies targeting FBP1 are discussed, including inhibitors, activators, epigenetic modulation, and combination therapies, while addressing the challenges posed by its dual nature. Understanding the multifaceted roles of FBP1 offers valuable insights into cancer metabolism and opens avenues for personalized therapeutic interventions.

Moreover, FBP1 knockdown reduced CD206 fluorescence intensity and the phosphorylation of STAT6. To conclude, FBP1 could be considered as a biomarker that affected the malignant phenotypes and aerobic glycolysis in GBM, contributing to the diagnosis and treatment of GBM.

This study suggests that the TyG index level before NACT is an independent prognostic factor for DFS and OS and can serve as a promising biomarker to predict the long-term prognosis of breast cancer patients undergoing NACT. Moreover, the TyG index and TyG-BMI show a linear correlation with DFS and OS. The effect of the TyG index on DFS and OS is not significantly mediated by lg-transformed BMI. Besides, FBP1 and G6PD are prognostic indicators for breast cancer patients and may serve as biomarkers for the clinical diagnosis and treatment of breast cancer.

Additionally, FBP1 inhibited the proliferation, apoptosis, and invasion of thyroid cancer cells by modulating HIF-1α expression. Our results provide new insights into the role of FBP1 in PTC progression and indicate that targeting the FBP1-HIF-1α axis could be a promising therapeutic approach for this disease.

Finally, the humanized immune system mouse models confirmed the above role of FBP1. Thus, FBP1 may serve as a new target to cure lung adenocarcinoma, and IL33 may improve the efficiency of immune therapy in lung adenocarcinoma.

These findings suggested that Huaier granules were capable of inhibiting CCA development through regulating the Twist1/FBP1/Wnt/β-catenin signalling axis and provided a novel orientation for the development of novel anti-CCA drugs.

The present study aimed to determine the function of KMT5A in inducing docetaxel (DTX) resistance in patients with breast carcinoma by evaluating glucose metabolism and the underlying mechanism involved...In conclusion, KMT5A was shown to affect chemotherapy resistance by regulating the cell cycle and positively regulate glycolysis‑mediated chemotherapy resistance by inhibiting the transcription of FBP1 in collaboration with TWIST1. KMT5A may be a potential therapeutic target for chemotherapy resistance in BRCA.