DLST (Dihydrolipoamide S-Succinyltransferase)

In this study, we found that DLST promotes the proliferation, migration, invasion, anti-apoptosis of osteosarcoma cells, as well as tumor growth, regulated through the p38 MAPK signaling pathway. These results could offer novel and valuable perspectives for the clinical management of osteosarcoma.

These findings establish that cuproptosis exacerbates ECM pathogenesis by promoting astrocyte reactivity, highlighting copper homeostasis modulation as a potential therapeutic strategy for CM.

Our findings suggests that DLST drives melanoma progression via both metabolic and epigenetic mechanisms, positioning it as a potential therapeutic target. This research offers a novel theoretical foundation for improving melanoma prognosis and treatment strategies.

HTR-8/SVneo cells were cultured in vitro and treated with Elesclomol, CuCl2 and/or TSA, tetrathiomolybdate (TTM)...TSA can promote oxidative stress in HTR-8/SVneo cells, leading to cell apoptosis. This process can be reversed by copper chelator.

Our research is the first to utilize machine learning techniques in identifying DLST and LSP1 as significant biomarkers of VTE. With our findings, we have uncovered new insights into the underlying causes of VTE and potential treatments for affected patients.

In addition, drug sensitivity analysis experiments suggest that erlotinib may be a potential treatment for high-risk patients. The results of in vitro experiments confirmed that DLD and DLST had higher expression levels in UM cell lines. The prognostic signature developed in this study is a reliable biomarker for predicting the prognosis of UM and may serve as a tool for personalised treatment of patients with UM.

A germline mutation in the dihydrolipoamide succinyltransferase (DLST) gene (c.330 + 14A>G) was detected, and despite trying chemotherapy and adjuvant therapy, the patient had a limited response with an overall survival of 27 months. DLST mutation is one of the rare pheochromocytoma-related mutated genes, and genetic sequencing is crucial for effective clinical management.

We discovered and validated a novel CRG signature with strong predictive capability for diagnosing MM, potentially implicated in MM pathogenesis and progression through immune-related pathways.

As a result, DLST targeting of aberrant glutamine metabolism will have the dual benefit of reducing CD11b+Gr1+ cell-mediated immunosuppression while also directly inhibiting tumor growth. Thus CPI-613 represents an attractive drug to target glutamine addiction and reduce immunosuppressive environment plaguing ovarian cancer.

Finally, we demonstrated that LINC02154 and our constructed risk signature could predict outcomes and have potential clinical value.

Transcriptional and methylation profiling and metabolite assessment showed an "intermediate signature" to suggest that both variants had a pathological role in tumour development. In conclusion, mutations affecting genes involved in different pathways (pseudohypoxic and receptor tyrosine kinase signalling) co-occurring in the same patient could provide a selective advantage for the development of PPGL, and explain the variable expressivity and incomplete penetrance observed in some patients.