FDPS (Farnesyl Diphosphate Synthase)

These findings suggest that FDPS may play a role in the survival and growth of endometrial cancer cells. This study provides new insights into the potential function of FDPS in the uterus and suggests that targeting FDPS may represent a promising therapeutic strategy for endometrial cancer.

In summary, this study highlights FDPs play an essential oncogenic role in HCC, linking it to metabolic reprogramming and tumour survival. These findings establish FDPs as a promising therapeutic target, offering a foundation for further exploration of its regulatory mechanisms and potential clinical applications.

934 out of 1136 mitochondrial proteins in the Human.MitoCarta3.0 database were differentially expressed in HCC, suggesting that mitochondrial proteins play an important biological role in the development of HCC. Further experimental validation and bioinformatics analyses showed that functional mitochondrial proteins are potential pathophysiological mechanisms for malignant progression of HCC. Mitochondrial proteins, in the future, have the potential to be valuable therapeutic targets for HCC.

This study highlights the influence of gut bacteria on host cholesterol synthesis. Targeted modulation of gut microbiota to reduce cholesterol may represent a promising preventive strategy for CRC.

ISO treatment may attenuate the pathological behaviours of RA FLS by targeting FDPS-mediated phosphorylation of AKT and ERK1/2 pathways. Our data suggest that ISO might be a novel potential agent for RA treatment.

TYE inhibits SQLE transcription to decrease its protein expression, reduces cholesterol biosynthesis and accumulation, impedes DNA damage repair, leading to cell cycle arrest, and thus elicits cell death, followed by obstruction of breast cancer progression. T. yunnanensis may be a novel anti-breast cancer agent owing to its inhibitory effects on cholesterol biosynthesis.

Our study illustrates that FDPs can cause aggregation of α-synuclein in MSA by inhibiting Beclin1-mediated autophagy, which may exacerbate disease progression. These results provide a new therapeutic approach for MSA, that targets the inhibitory effect of FDPs on oligodendrocyte autophagy.

In conclusion, ZA preserved renal function and prevented renal fibrosis in a rat model. These were achieved through targeting protein prenylation mainly by inhibiting FPPS.

Differential expression and gene set enrichment analysis in TNBC revealed enrichment in the cycle and mitosis functional categories in FDPS, while ENO1 was associated with numerous functional categories, including cell cycle, glycolysis, and ATP metabolic processes. Taken together, our data are the first to unravel the unique gene signatures and to identify novel dependencies and therapeutic vulnerabilities for each BC molecular subtype, thus setting the foundation for the future development of more effective targeted therapies for BC.

FDPS also affected the cell proliferation rate. These findings broaden the understanding of the molecular functions of FDPS, and the potential of FDPS as a target in therapy should be investigated.

This data-driven MR study demonstrated the causal role of mitochondrial dysfunction in multiple cancers. Furthermore, this study identified candidate genes that can be the targets of potential pharmacological agents for cancer prevention.

Our bioinformatics analysis revealed 7 hub genes derived from the specific DEGs between the MSCs and osteoblastic cells. The 7 hub genes may serve as potential prognostic biomarkers for patients with OS.