Advances in the study of disulfidptosis in digestive tract tumors

Discover Oncology, Journal Year: 2025, Volume and Issue: 16(1)

Published: Feb. 15, 2025

Disulfidptosis, a recently identified cell death mechanism, plays pivotal role in the development, progression, and treatment of digestive tract tumors, including gastric cancer, hepatocellular esophageal colorectal pancreatic cholangiocarcinoma, neuroendocrine which have high global incidence mortality rates. Analyzing expression disulfidptosis-related gene within tumor microenvironment enhances our understanding biology facilitates novel diagnostic therapeutic strategies. Research on immune infiltration checkpoints can identify targets linked to disulfidptosis, thereby improving immunotherapy efficacy. Targeting genes such as SLC7A11, are essential for maintaining glutathione levels regulating oxidative stress, may overcome chemoresistance enhance existing treatments. Disulfidptosis could complement current therapies it induces cytoskeletal collapse selective death, especially chemoresistant cancers. Additionally, like RPN1, NCKAP1 cancer correlate with poor prognosis, highlighting their potential prognostic biomarkers. Personalized medicine approaches utilizing biomarkers patients who would benefit from targeting stress regulation, leading more precise treatments improved outcomes. This review summarizes disulfidptosis mechanisms, advancements cancers, related response evaluation, targeted therapies, providing perspectives diagnosis personalized treatment.

Language: Английский

Disulfidptosis in tumor progression

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: April 28, 2025

Abstract Disulfidptosis, a regulated cell death modality driven by the cystine transporter solute carrier family 7 member 11 (SLC7A11), is characterized actin cytoskeleton collapse under glucose starvation. This review systematically elucidates pivotal role of disulfidptosis in tumor metabolic reprogramming, with focus on its molecular mechanisms and distinctions from other pathways. The core include SLC7A11-mediated overload NRF2/c-Myc-regulated pentose phosphate pathway activation. By integrating multiomics data single-cell transcriptomics, we comprehensively decipher heterogeneous expression patterns disulfidptosis-related genes (DRGs) their dynamic interplay immune microenvironment remodeling. Furthermore, coexpression networks DRGs long noncoding RNAs (DRLs) offer novel insights into diagnosis, prognosis, targeted therapy. Therapeutically, SLC7A11 inhibitors (e.g., HG106) BAY-876) demonstrate efficacy exploiting vulnerabilities, whereas natural compounds synergizing checkpoint blockade provide strategies to counteract immunosuppressive microenvironments. Through interdisciplinary collaboration clinical translation, research holds transformative potential redefining precision oncology.

Language: Английский

Disulfidoptosis: A New Key to Unlocking Cancer Treatment

Cell Biochemistry and Function, Journal Year: 2025, Volume and Issue: 43(5)

Published: May 1, 2025

ABSTRACT The metabolic properties of disulfidoptosis targeting cancer cells have become a new key to unlocking treatment's lock. Conventional therapies aim kill tumor through apoptosis, but cell death is carried out by network cascading enzymes. Malignant can evade the process downregulating enzymes or inhibiting death‐inducing triggers, leading persistence and recurrence that are resistant conventional immune escape, which has compelled researchers explore therapeutic avenues. Disulfidoptosis triggered accumulation excessive intracellular disulfides in with high expression solute carrier family 7 member 11 (SLC7A11) under glucose starvation conditions, simultaneously induces breakage disulfide bonds leads protein malfunction, thereby triggering death. However, there no comprehensive account application therapy. This review comprehensively summarizes mechanism for treatment, provides ideas treatment.

Language: Английский