AMBRA1 (Autophagy And Beclin 1 Regulator 1)

WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

Immunohistochemical analysis distinguished two patterns: high LONP1/low TOMM20 expression associated with aggressive tumors and low LONP1/high TOMM20 expression linked to better outcomes and stronger immune infiltration. These findings suggest that LONP1 contributes to tumor progression through mitochondrial regulation and immune modulation, highlighting its potential as both a prognostic biomarker and a therapeutic target in COAD.

These findings offer insights into PPGL molecular mechanisms, suggest prognostic biomarkers, and propose candidate therapeutic targets to improve risk stratification and personalized treatment. However, experimental validation is required to confirm their biological relevance before clinical application.

mTOR or caloric-restriction mimetics jump-start a protective flux; chloroquine derivatives and ULK1 blockers clip tumour survival circuits; cannabinoids, photodynamic therapy and immune-checkpoint combinations exploit context-specific toggling between induction and brake. Emerging biomarkers (LC3B-II, p62, AMBRA1) promise patient-stratified interventions. By weaving together molecular detail, pre-clinical insight and clinical translation, we show why autophagy is no longer a backstage process but a star player in dermatology - and how targeting its switches could reshape future treatment algorithms.

The ERLIN1/2 complex also influences immune responses and viral replication through cholesterol regulation. Collectively, these diverse and integrated functions highlight the potential of ERLIN1 as a therapeutic target in cancer, metabolic, neurodegenerative, and infectious diseases.

Ambra1 can control the proliferation of BC cells by regulating the Akt-FoxO1-p27 signaling pathway. Therefore, this protein is a potential therapeutic target for BC.

In contrast, overexpression of LZTR1 provides growth advantage under environmental stress, enhancing cell invasion, by activating ERBB3 receptor and its downstream targets PYK2 and SRC tyrosine kinases that regulate the cytoskeleton, actin organization, cell spreading, cell migration and adhesion. LZTR1 is a "safeguard" for melanoma cells under stress and its downregulation can be exploited for melanoma therapy.

Notably, their susceptibility to spontaneous, radiation-, and chemically induced malignancies was significantly higher. These findings support the role of AMBRA1 as a tumor suppressor that regulates cyclin Ds, although other targets may also contribute.

METTL3 promotes MCL progression through YTHDF2-mediated degradation of Ambra1 mRNA, suggesting that the METTL3/YTHDF2/Ambra1 may serve as a potential therapeutic target for MCL.

Importantly, we identified two LDHA inhibitors, triflupromazine (TRI) and tranylcypromine (TRA), that significantly improve cisplatin efficacy both in vitro and in vivo. These findings highlight a critical role of LDHA in promoting cisplatin resistance, and suggest that targeting LDHA may represent a promising therapeutic strategy for patients with advanced LUAD.

Silencing p53 or overexpressing CDK2 reversed the repressive effects of AMBRA1 on the development of NSCLC cells. AMBRA1 may suppress the malignant phenotype of NSCLC cells via regulating the miR-1178-p53-CDK2 signalling pathway.

In addition, we show that AMBRA1 mutants, which are defective in cyclin D1 binding, lead to cyclin D1 accumulation and DNA damage. Understanding the AMBRA1-D-type cyclin structure enhances the knowledge of the molecular mechanisms that govern the cell cycle control and may lead to potential therapeutic approaches for cancers linked to abnormal cyclin D activity.