HMGCS1 (3-Hydroxy-3-Methylglutaryl-CoA Synthase 1)

CuHL1 exhibits potent cytotoxicity in the low micromolar range (IC50 ≈ 2 µM), surpassing cisplatin by up to 81-fold...Functional assays confirm reduced migratory capacity in MDA-MB-231 cells. These findings position CuHL1 as a promising candidate for TNBC therapy, meriting further in vivo evaluation.

In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets.

Additionally, SLD regulated key signaling pathways including peroxisome proliferator-activated receptor(PPAR), tumor protein P53(P53), and Hippo. Further studies revealed that SLD activated the PPAR signaling pathway by upregulating key targets such as peroxisome proliferator-activated receptor δ(PPARδ) and fatty acid desaturase 2(FADS2) and downregulating Acyl-CoA synthetase long chain family member 3(ACSL3) and 3-hydroxy-3-methylglutaryl-CoA synthase 1(HMGCS1), which promoted fatty acid β-oxidation, inhibited fatty acid synthesis, improved hepatic lipid metabolism, and ultimately exerted the effects of protecting liver function and alleviating liver injury.

VK1 has cytotoxic effects and transcriptional regulation of multiple genes on Jurkat T cells. The genes of HMGCR and HMGCS1 related pathways may play roles in this process.

This study clarified a specific signature associated with fatty acid metabolism, specifically FASN, which is connected to both the initiation and progression of CESC. Furthermore, FASN may serve as a prognostic marker for individuals diagnosed with CESC, thus providing fresh insights for the formulation of clinical treatment strategies.

Additionally, ferroptosis induction via radiotherapy, natural compounds (solasodine, luteolin), repurposed drugs (disulfiram/copper), or nanotechnology synergizes with immunotherapy by promoting lipid peroxidation and reversing EBV-mediated immune evasion. Targeting ferroptosis regulators (SLC7A11, GPX4, FTO, CD38) overcomes resistance, positioning ferroptosis modulation as a transformative strategy for NPC management.

CRC cells with hyper-expressed HMGCS1 facilitated M2-like TAM polarization by releasing cholesterol-rich EVs, and M2-like TAMs in turn promoted CRC malignancy. These findings suggest that inhibiting excessive cholesterol production may be a promising strategy for the treatment of advanced CRC.

The results of this study indicate that the reduction in cholesterol levels observed in breast cancer cells following IGFBP6 knockdown is primarily due to decreased exogenous uptake. These findings highlight the role of IGFBP6 in regulating cholesterol metabolism and further explain its clinical significance in predicting breast cancer recurrence and progression.

Finally, we find that while Hymeglusin is a valuable tool for short-term mechanistic studies, its usefulness is limited for long-term efficacy studies due to its poor stability in serum. Together, this study highlights the biological implications of targeting HMGCS1 as monotherapy or in combination with statins, and caution is required when using Hymeglusin as a tool.

The effect of HuR on the stability of splicing factor proline- and glutamine-rich (SFPQ) mRNA was verified by dual-luciferase reporter gene assay and actinomycin D treatment...RNA sequencing analysis indicated that SFPQ may inhibit apoptosis by suppressing tumor necrosis factor (TNF) signaling. This study revealed that circHMGCS1 contributes to NSCLC progression by stabilizing oncogenic HuR and promoting post-transcriptional upregulation of SFPQ, highlighting its potential as a diagnostic and prognostic biomarker for NSCLC.

On the contrary, overexpression of EBLN3P facilitated these cellular processes. The EBLN3P/miR-141-3p/HMGCS1 axis was identified to play crucial functions in GC progression.