ACSM3 (Acyl-CoA Synthetase Medium Chain Family Member 3)

This deep learning model demonstrated excellent performance in multi-omics subtype predictions. In, conclusion, this study systematically elucidates the molecular heterogeneity of LUAD through a multi-omics integration strategy, establishes a clinically relevant molecular classification system, and provides a theoretical foundation for developing personalized treatment plans for LUAD.

In this study, we propose that an AREG-based signature comprising ACSM3, ACTG2, and DES effectively predicts prognosis and reflects immune microenvironment characteristics in PRAD. Through systematic analysis, we established a prognostic model utilizing these three AREGs, which demonstrates strong potential as a clinical predictor for PRAD patient outcomes.

ACSM3 functions as a tumor suppressor in breast cancer by regulating the WNT/AKT signaling pathway, thereby inhibiting cell proliferation, migration, and invasion. These results suggest that ACSM3 may serve as a potential therapeutic target for breast cancer treatment.

This study highlights the diagnostic and prognostic significance of ACSM3 and describes the METTL14/ACSM3/GATA5/ HMGCS2/mTORC1 axis in a comprehensive study of ccRCC. These results provide a solid basis for research on ccRCC to explore new diagnostic and treatment strategies.

Moreover, treatment with interferon-gamma (IFN-γ) in A2780 cells reversed the effects of ACSM3 on cell proliferation, migration, invasion, and apoptosis, but IFN-γ further enhanced the effects of ACSM3 knockdown on SKOV3 cell proliferation, migration, invasion, and apoptosis. In conclusion, ACSM3 inhibited OC cell proliferation, migration, and invasion, and promoted cell apoptosis by suppressing the IFN-γ/JAK/STAT3 signaling pathway, which might provide a promising therapeutic target for OC treatment.

We established a novel prognostic mitochondria-related signature by machine learning algorithm, which also demonstrated outstanding predictive value in tumor microenvironment and responses to therapies.

Conversely, elevated ACSM1/3 activity enabled prostate cancer cells to survive toxic levels of medium chain fatty acids and promoted resistance to ferroptosis-inducing drugs and AR antagonists. Collectively, this study reveals a tumor-promoting function for medium chain acyl-CoA synthetases and positions ACSM1 and ACSM3 as key players in prostate cancer progression and therapy resistance.

In contrast, the copy number gain in fewer genes, including NRXN3, ZNF667, ACSM3, C6, ADCY5, SCN9A, and PRKCE, is significantly associated with changes in immune cell infiltrates. Our study suggested that neuronal development genes play a role in modulating TME in a pancreatic cancer setting.

We found that ACSM3 was regulated by IGF2BP3 and attenuated BRCA proliferation, invasion and stem cell properties. The role of ACSM3 in BRCA was first revealed, which provides a novel target for treatment.

Our findings revealed the expression patterns, prognostic, and diagnostic biomarker potential of ACS enzymes in colon adenocarcinoma. ACSM3, ACSM5, ACSS2, and ACSF2 genes are suggested as possible prognostic and diagnostic biomarkers.

Furthermore, copy number variation was bound up with the 8 prognostic genes in expression levels. We have preliminarily determined the prognostic value of MMRGs in HGSOC as well as relationship between MMRGs and the tumor immune microenvironment.

mRNA stabilization of ACSM3 following actinomycin D treatment was evaluated using reverse transcription-quantitative PCR analysis...In addition, IGF2BP2 overexpression counteracted the effects of ACSM3 overexpression noted on proliferation, induction of apoptosis and cell cycle arrest of HL-60 cells. In conclusion, ACSM3 repressed the cell proliferative activity and facilitated induction of apoptosis and cell cycle arrest in AML cells by modulating the expression of IGF2BP2.