Dichotomous roles of ACBD3 in NSCLC growth and metastasis DOI Creative Commons
Xiaochao Tan, Chao‐Liang Wu, Priyam Banerjee

et al.

Oncogene, Journal Year: 2025, Volume and Issue: unknown

Published: April 6, 2025

Abstract Lung cancer continues to be the leading cause of cancer-related deaths globally. Unraveling regulators behind lung growth and its metastatic spread, along with understanding underlying mechanisms, is crucial for developing novel effective therapeutic strategies. While much research has focused on identifying potential oncogenes or tumor suppressors, roles certain genes can vary depending context may even exhibit contradictory effects. In this study, we demonstrate that acyl-CoA binding domain containing 3 (ACBD3), a Golgi resident protein, promotes primary by recruiting phosphatidylinositol (PI)-4-kinase IIIβ (PI4KB) Golgi, thereby enhancing oncogenic secretion in chromosome 1q-amplified cells. Conversely, 1q-diploid cells, ACBD3 acts as suppressor metastasis inhibiting NOTCH signaling pathway reducing cell motility. This highlights intricacy progression cautions against simplistic approaches targeting individual therapy.

Language: Английский

Piwei Peiyuan Prescription Attenuates the Progression of Chronic Atrophic Gastritis by Eliciting MAPK10‐Mediated Mitochondrial Autophagy DOI Open Access
Yi Zhang, Ying Wu, Bei Pei

et al.

Cell Biology International, Journal Year: 2025, Volume and Issue: unknown

Published: March 18, 2025

ABSTRACT Piwei Peiyuan (PWPY) prescription is a traditional Chinese medicine and has been efficiently used in the clinics to treat chronic atrophic gastritis (CAG) for many years. However, mechanism of action underlying PWPY treating CAG remains elusive. A rat animal cell model was constructed this study explore CAG. Here we show that attenuates progression by eliciting MAPK10‐mediated mitochondrial autophagy. Experimental introduced using N ‐methyl‐n'‐nitro‐n‐nitroguanidine (MNNG). Our histological analyses reveal MNNG‐induced undergoes classical morphological alterations judged immunohistochemistry serum level PGⅠ, PGⅡ, G17. Importantly, treatment prevents Interestingly, inhibits MAPK10 activity biochemical assays promotes autophagy electron microscopic analyses. Thus, conclude precancerous lesions harnessing MAPK10‐elicited The experimental provides robust platform further delineating therapeutic targets regimen.

Language: Английский

Citations

0

Exploring Ferroptosis in Allergic Inflammatory Diseases: Emerging Mechanisms and Therapeutic Perspectives DOI
Henry Sutanto,

Laras Pratiwi,

Deasy Fetarayani

et al.

Cell Biology International, Journal Year: 2025, Volume and Issue: unknown

Published: April 22, 2025

ABSTRACT Ferroptosis, a unique form of regulated cell death driven by iron accumulation and lipid peroxidation, has emerged as critical process in various diseases. Recent evidence suggests its involvement the pathogenesis allergic diseases, including asthma, rhinitis, atopic dermatitis. These conditions are characterized chronic inflammation, oxidative stress, immune dysregulation, all which intersect with molecular mechanisms ferroptosis. Key regulators, such glutathione peroxidase 4 (GPX4), cystine/glutamate antiporter system Xc‐, metabolism pathways, play pivotal roles ferroptotic processes their contribution to disease progression. This review explores mechanistic link between ferroptosis emphasizing how damage overload exacerbate inflammation tissue injury. We also highlight emerging diagnostic biomarkers, peroxidation products could improve monitoring stratification. Therapeutic strategies targeting ferroptosis, GPX4 activators, chelators, inhibitors, show promise preclinical\ studies, offering potential new avenues for treating However, challenges remain translating these findings into clinical applications. By integrating current knowledge, this underscores need further research both biomarker therapeutic target

Language: Английский

Citations

0

Dichotomous roles of ACBD3 in NSCLC growth and metastasis DOI Creative Commons
Xiaochao Tan, Chao‐Liang Wu, Priyam Banerjee

et al.

Oncogene, Journal Year: 2025, Volume and Issue: unknown

Published: April 6, 2025

Abstract Lung cancer continues to be the leading cause of cancer-related deaths globally. Unraveling regulators behind lung growth and its metastatic spread, along with understanding underlying mechanisms, is crucial for developing novel effective therapeutic strategies. While much research has focused on identifying potential oncogenes or tumor suppressors, roles certain genes can vary depending context may even exhibit contradictory effects. In this study, we demonstrate that acyl-CoA binding domain containing 3 (ACBD3), a Golgi resident protein, promotes primary by recruiting phosphatidylinositol (PI)-4-kinase IIIβ (PI4KB) Golgi, thereby enhancing oncogenic secretion in chromosome 1q-amplified cells. Conversely, 1q-diploid cells, ACBD3 acts as suppressor metastasis inhibiting NOTCH signaling pathway reducing cell motility. This highlights intricacy progression cautions against simplistic approaches targeting individual therapy.

Language: Английский

Citations

0