This mitochondrial ferroptosis-based risk model represents a promising prognostic biomarker and may offer valuable insights for personalized treatment strategies in colon cancer management. P4HA1 facilitates the advancement of colorectal cancer, while its suppression diminishes the in vitro proliferation and migration of colorectal cancer cells.
Although GDF15 expression was decreased in CRPC cells, overexpression of GDF15 still facilitates CRPC cells migration and invasion in vitro. Our findings suggest that this novel FRGs signature and GDF15 could be robust biomarkers for predicting CRPC in clinical practice.
8 months ago
Journal
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GDF15 (Growth differentiation factor 15) • ABCC5 (ATP Binding Cassette Subfamily C Member 5) • Pdss2 (Prenyl (solanesyl) diphosphate synthase subunit 2) • ZFP36 (ZFP36 Ring Finger Protein) • ACSL1 (Acyl-CoA Synthetase Long Chain Family Member 1)
Our study elucidates a novel molecular mechanism by which PDSS2-Del2 promotes HCC metastasis, which may contribute to the development of effective HCC clinical treatment and prevent tumor metastasis. Furthermore, MST1 could be a potential therapeutic target, and MST1 inhibitors might be integrated into clinical practice for HCC patients with high expression of PDSS2-Del2.
Enforcing synthesis of coenzyme Q through deletion of Fdft1 or overexpression of PDSS2 promoted mitochondrial respiration, memory T cell formation following viral infection and enhanced antitumour immunity. In sum, through a systematic exploration of T cell metabolism, we reveal how these programs can be leveraged to fuel memory CD8 T cell formation in the context of acute infections and enhance antitumour immunity.
The levels of PDSS2 expression were significantly decreased in lung cancer samples, and lung cancer patients with high expression of SKA2 and low expression of PDSS2 displayed remarkable poor prognosis. Collectively, our results demonstrated that PDSS2 is a novel downstream target gene of SKA2 in lung cancer cells, and the SKA2-PDSS2 transcriptional regulatory axis functionally contributes to human lung cancer cell malignant phenotypes and prognosis.
Moreover, lower level of mitochondrial DNA-encoded cytochrome c oxidase subunit 2 was not only associated with a higher malignancy degree but also with lower level of all COQ proteins detected. The results revealed that mitochondrial abnormalities are associated with impaired CoQ maintenance in human astrocytoma progression.
In contrast, arginine biosynthesis was correlated with sensitivity to HSP90 inhibitors. Further study of these outcomes could enable the development of strategies to improve the clinical efficacy of HSP90 inhibition in patients with lung adenocarcinoma.
Considering that DMF is a prescribed oral therapy for multiple sclerosis, it might be a potential treatment for metastasis of patients with HCC. Early clinical trials are needed to validate its potential in this context.
Of note, the expression of Sp1 and PDSS2 are negatively correlated, and higher Sp1 expression with low PDSS2 expression is significantly associated with poor prognosis in lung cancer. Taken together, our results strongly suggest the essential role of Sp1 in maintaining the basic constitutive expression of PDSS2, and the pathogenic implication of Sp1-mediated PDSS2 transcriptional repression in lung cancer cells.