FBXO32 (F-Box Protein 32)

Moreover, increased oxidative stress and oxidative stress-sensitive casitas B-lineage lymphoma proto-oncogene-b (Cbl-b) ubiquitin ligase induced by Dex were effectively diminished by HMPA/HMCA administration. These observations suggest that HMPA and HMCA may be potential in vivo therapeutic agents that attenuate muscle atrophy by reversing atrophy-mimicking genes, oxidative stress, and related anomalies.

Our study has shown that FBXO32 facilitates HCC growth and metastasis via the PTEN/PI3K/AKT signaling through ubiquitination of TAL1. Consequently, FBXO32 emerges as a promising target for therapeutic intervention in the treatment of HCC.

Specifically, exercise can enhance muscle protein synthesis by activating the mTOR pathway while reducing protein degradation by suppressing the expression of muscle atrophy genes. In this narrative review, we summarize the mechanisms of action of the genes associated with muscle atrophy, MuRF-1 and ATROGIN-1, and their differential expression patterns following experimental and clinical trials involving chronic and acute exercise exposure, along with other potential regulators implicated in muscle remodeling.

Furthermore, in muscle cells, MCC950 directly silences NLRP3 inflammasome signaling, inhibits pyroptosis and IL-1β/IL-18 secretion, suppresses muscle protein degradation to rescue cancer cachexia-driven muscle atrophy. These findings revealed the important role of NLRP3 inflammasome in cancer cachexia and also suggested the possibility of developing NLRP3 inflammasome inhibitors such as MCC950 to be novel therapeutic candidates for cancer cachexia treatment.

This study examined the effects of five anticancer agents-cisplatin, 5-fluorouracil, vincristine, irinotecan, and cyclophosphamide-on mouse skeletal muscle. Targeting ER stress may help prevent chemotherapy-induced muscle wasting. Further studies are needed to clarify mechanisms and develop protective strategies.

Our findings underscore the critical role of TLR4 signalling in cachexia-associated muscle wasting across different disease contexts and demonstrate the efficacy of OH-CATH30, a TLR4 inhibitor, in alleviating muscle atrophy in various cachexia models.

In this model, ICI-induced cardiotoxicity was characterized by severe cardiac remodeling and dysfunction, associated with dysfunctional metabolism, muscle wasting, and autophagy. To our knowledge, this is one of the first studies to explore underlying pathological mechanisms, adding novel and impactful insight to the still unclear characteristics of ICI-induced cardiotoxicity and supporting the critical need to further investigate side effects of immunotherapies to optimize clinical treatment of cancers.

Moreover, IGFBP-3 deletion in tumor cells and small molecule inhibition of TGF-βR1/2 attenuated myotube wasting. Collectively, these results suggest that PDAC derived IGFBP-3 promotes SMW via non-canonical binding of TGF-βRs, warranting formal investigation of IGFBP-3 as a potential therapeutic target for PDAC-related SMW through a novel pathway.

The limited efficacy and adverse effects of synthetic agents like megestrol acetate underscore the value of herbal therapies as safer adjunctive strategies...While promising, current evidence remains largely preclinical and mechanistic validation is incomplete. This review consolidates contemporary insights into CC pathogenesis and the bioactivity of herbal interventions, highlighting the need for translational research to bridge preclinical findings with clinical applicability.

METTL3/YTHDF1 aggravated UC progression through promoting M1 macrophage polarization via SerpinB5 mRNA m6A modification and FBXO32/NF-κB pathway. These findings indicated that SerpinB5 might be a good and promising therapeutic target for UC treatment.

IGF2BP3 increases FBXO32 protein expression in an m6A-dependent manner, activates the cGMP-PKG signaling pathway, and promotes GC progression. Targeting of the IGF2BP3/FBXO32/cGMP-PKG axis could thus represent a promising therapeutic modality for GC.

This study identified and validated four EM-related prognostic biomarkers in neuroblastoma, with GNG12 functionally implicated in tumor cell proliferation and migration. These findings provide potential therapeutic targets and prognostic indicators for neuroblastoma management.