An MITF- and mTOR-dependent FLCN pathway suppresses TFE3-driven metastasis in melanoma DOI Creative Commons
Jeremy Chang,

Katelyn R Campbell-Hanson,

Marion Vanneste

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июль 12, 2024

Cancer cells have remarkable plasticity allowing them to acquire many biological states. Melanoma the ability switch from a proliferative melanocytic state an invasive mesenchymal and back again resulting in intratumoral heterogeneity. While microphthalmia-associated transcription factor (MITF) promotes phenotype, it is unclear what factors drive mechanisms regulate state. We show that nuclear localization of MITF paralog TFE3 correlates positively with metastatic potential melanoma cell lines tumors, deletion MITF-low eliminates migration ability. Further, we find suppresses phenotype by activating expression FNIP2, which encodes component mTORC1-stimulated pathway promoting cytoplasmic retention lysosomal degradation TFE3. These findings point mTOR as key regulators plasticity.

Язык: Английский

The effects of autophagy-modifying drugs chloroquine and lithium on the skin melanoma microenvironment DOI
Iuliia Taskaeva,

Anastasia Shatruk,

Igor Ivanov

и другие.

Tissue and Cell, Год журнала: 2025, Номер 93, С. 102753 - 102753

Опубликована: Янв. 20, 2025

Язык: Английский

Процитировано

0
mTORC1 regulates the proliferation of SOX9+ porcine skin-derived stem cells (pSDSCs) by promoting S6K phosphorylation DOI

Ming-Xin Zang,

Geng Zhang,

Ying Zhang

и другие.

Histochemistry and Cell Biology, Год журнала: 2025, Номер 163(1)

Опубликована: Янв. 20, 2025

Язык: Английский

Процитировано

0
DPHB inhibits osteoclastogenesis by suppressing NF-κB and MAPK signaling and alleviates inflammatory bone destruction DOI
Caixia Liu,

Min Zuo,

Jing Zhao

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 152, С. 114377 - 114377

Опубликована: Март 4, 2025

Язык: Английский

Процитировано

0
Antagonistic roles for MITF and TFE3 in melanoma plasticity DOI
Jeremy Chang,

Katelyn R Campbell-Hanson,

Marion Vanneste

и другие.

Cell Reports, Год журнала: 2025, Номер 44(4), С. 115474 - 115474

Опубликована: Март 27, 2025

Язык: Английский

Процитировано

0
Bibliometric analysis of autophagy in the diagnosis and treatment of osteosarcoma: a bibliometric analysis (2007–2023) DOI Creative Commons
Min Zhu, Wei Xiang,

Zhoujun Zhu

и другие.

Cancer Biology & Therapy, Год журнала: 2025, Номер 26(1)

Опубликована: Март 27, 2025

Osteosarcoma is the most common primary bone tumor in children and adolescents. Its pathogenesis complex poses difficulties treatment. Autophagy a cell biological process that plays crucial role mechanistic study treatment of osteosarcoma. The objective this to evaluate past research progress from 2007 2023 visualize key directions through bibliometric methods. Relevant publications published start end were searched screened Web Science Core Collection. They analyzed visualized using CiteSpace Bibliometric online analysis platform terms country, institution, author, journal, cited references, keywords. In total, 619 522 journals with 682 authors 42 countries screened. country highest number China (n = 445, 71.890%), followed by United States 60, 9.693%). institution Shanghai Jiao Tong University 42, 6.785%). author Cai, Zhengdong 7), while Mizushimma N 93). Among many journals, AUTOPHAGY has citations 342), CANCER LETT shows greatest centrality (Centrality 0.05). "Autophagy" keyword 177), largest burst intensity "cancer cells" (Strength 6.27), which lasted 2011 2014. major contributor autophagy field osteosarcoma, States. All are high-quality journals. hot topic field.

Язык: Английский

Процитировано

0
Artesunate-driven autophagy: a shield against liver hypoxia/reoxygenation insult in rats via modulation of GLP1R, the chief metabolic kinase AMPK, mTOR, ULK1, P70S6K, cyclin D1, Akt, and GSK3β DOI Creative Commons
Mai El-Sayed Ghoneim, Hanan S. El‐Abhar, Dalaal M. Abdallah

и другие.

Future Journal of Pharmaceutical Sciences, Год журнала: 2024, Номер 10(1)

Опубликована: Окт. 11, 2024

Abstract Background Hepatic hypoxia/reoxygenation (H/R) insult is a critical issue in hepatic transplant and surgeries, profoundly influencing postoperative prognosis. One crucial pathomechanism this condition impaired autophagy flux, which disrupts liver homeostasis. Artesunate, an antimalarial drug, has shown potential providing hepatoprotection against H/R injury; however, whether it can modulate disrupted to enhance remains unclear. Purpose of the study Accordingly, we delved into mechanism(s) through artesunate modulates process injury model. Methods results Rats were categorized three groups, viz. sham operated, H/R, artesunate-treated (50 mg/kg, i.p). Disease regression was evaluated microscopically, molecular alternations assessed biochemically using ELISA western blotting techniques. Mechanistic analysis revealed that administration at reperfusion time significantly upregulated gene expression GLP1R protein p -AMPK, accompanied by downregulation those -mTOR, its target molecule -ULK1, presenting first trail initiate autophagy. Additionally, reduced H/R-induced -mTOR/P70S6K cue, cyclin D1 content, positively correlated with mTOR/P70S6K axis. Moreover, sharply active -Akt, turn phosphorylated/inactivated GSK3β, cascade indirectly promotes Consequently, increased beclin-1 LC3-II further uphold autophagic capacity. The hepato-therapeutic effectiveness evidenced serum ALT AST levels, along diminished histopathological alterations. Conclusion Artesunate protected triggering partly modulating GLP1R/AMPK/mTOR/ULK1, GLP1R/AMPK/mTOR/P70S6K, D1, Akt/GSK3β trajectories significant therapeutic managing insult.

Язык: Английский

Процитировано

1
An MITF- and mTOR-dependent FLCN pathway suppresses TFE3-driven metastasis in melanoma DOI Creative Commons
Jeremy Chang,

Katelyn R Campbell-Hanson,

Marion Vanneste

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июль 12, 2024

Cancer cells have remarkable plasticity allowing them to acquire many biological states. Melanoma the ability switch from a proliferative melanocytic state an invasive mesenchymal and back again resulting in intratumoral heterogeneity. While microphthalmia-associated transcription factor (MITF) promotes phenotype, it is unclear what factors drive mechanisms regulate state. We show that nuclear localization of MITF paralog TFE3 correlates positively with metastatic potential melanoma cell lines tumors, deletion MITF-low eliminates migration ability. Further, we find suppresses phenotype by activating expression FNIP2, which encodes component mTORC1-stimulated pathway promoting cytoplasmic retention lysosomal degradation TFE3. These findings point mTOR as key regulators plasticity.

Язык: Английский

Процитировано

0