USP20 mediates malignant phenotypic changes in bladder cancer through direct interactions with YAP1 DOI Creative Commons

Wenwen CHEN,

Siqi Wu,

Yifan Chen

et al.

Neoplasia, Journal Year: 2024, Volume and Issue: 60, P. 101102 - 101102

Published: Dec. 13, 2024

Language: Английский

New hope for the world cancer day DOI Creative Commons
Gerry Melino, Julia Bischof, Wen‐Lian Chen

et al.

Biology Direct, Journal Year: 2025, Volume and Issue: 20(1)

Published: Feb. 4, 2025

Language: Английский

Citations

1
The methionine cycle and its cancer implications DOI
Valentina Tassinari, Jia Wang, Wen‐Lian Chen

et al.

Oncogene, Journal Year: 2024, Volume and Issue: 43(48), P. 3483 - 3488

Published: Oct. 11, 2024

Language: Английский

Citations

4
The emerging significance of the METTL family as m6A-modified RNA methyltransferases in head and neck cancer DOI
Ming Yang,

Zile Zhang,

Hao Qin

et al.

Cellular Signalling, Journal Year: 2025, Volume and Issue: unknown, P. 111798 - 111798

Published: April 1, 2025

Language: Английский

Citations

0
Methionine Dependency and Restriction in Cancer: Exploring the Pathogenic Function and Therapeutic Potential DOI Creative Commons

Chi Ma,

Aoshuang Xu,

Liping Zuo

et al.

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(5), P. 640 - 640

Published: April 28, 2025

Methionine, an essential amino acid, is obtained by dietary intake to fulfill the requirements of our bodies. Accumulating evidence indicates that methionine plays a pivotal role in various biological processes, including protein synthesis, energy metabolism, redox balance maintenance, and methylation modifications. Numerous advances underscore heightened dependence cancer cells on methionine, which significant factor pathogenesis development. A profound comprehension intricate relationship between metabolism tumorigenesis imperative for advancing field therapeutics. Herein, we delve into supporting growth, impact epigenetic modifications, interaction tumor microenvironment. Additionally, provide insights development methionine-targeted therapy strategies. This paper summarizes current state research its translational potential, emphasizing challenges opportunities associated with harnessing as target innovative treatments.

Language: Английский

Citations

0
METTL3-Driven m6A Modifications in Esophageal Squamous Cell Carcinoma: Emerging Mechanisms, Biomarker Potential, and Therapeutic Innovations DOI
Ho-Kyung Chun,

Kangzhuo Baima

European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 177785 - 177785

Published: May 1, 2025

Language: Английский

Citations

0
Metabolic reprogramming in esophageal squamous cell carcinoma DOI Creative Commons
Ziyi Wang, Xiangyu Sun, Zehui Li

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: June 26, 2024

Esophageal squamous cell carcinoma (ESCC) is a malignancy with high incidence in China. Due to the lack of effective molecular targets, prognosis ESCC patients poor. It urgent explore pathogenesis identify promising therapeutic targets. Metabolic reprogramming an emerging hallmark ESCC, providing novel perspective for revealing biological features ESCC. In hypoxic and nutrient-limited tumor microenvironment, cells have reprogram their metabolic phenotypes fulfill demands bioenergetics, biosynthesis redox homostasis cells. this review, we summarized that involves glucose metabolism, lipid amino acid metabolism how reprogrammed provokes opportunities biomarkers potential targets

Language: Английский

Citations

3
Methionine deprivation inhibits glioma proliferation and EMT via the TP53TG1/miR-96-5p/STK17B ceRNA pathway DOI Creative Commons

Jiafeng Li,

Ruijie Liu, Hong Hu

et al.

npj Precision Oncology, Journal Year: 2024, Volume and Issue: 8(1)

Published: Nov. 21, 2024

Recent research highlights the significant impact of methionine metabolism on glioma progression. An increasing amount compelling evidence bridges long non-coding RNAs to abnormal in gliomas. However, specific role regulating progression remains unclear. This study reveals that deprivation inhibits proliferation, migration, and invasion capabilities Interestingly, expression TP53TG1, a RNA, is also suppressed. TP53TG1 highly expressed gliomas associated with poor patient outcomes. Subsequently, our data proves inhibition suppresses cell proliferation epithelial-mesenchymal transition process both vitro vivo. Ultimately, we found underlying mechanism involves competing endogenous RNA network, which modulates target protein STK17B by competitively binding miR-96-5p, thus These findings suggest targeting could be promising approach for clinical treatment glioma.

Language: Английский

Citations

2
USP20 mediates malignant phenotypic changes in bladder cancer through direct interactions with YAP1 DOI Creative Commons

Wenwen CHEN,

Siqi Wu,

Yifan Chen

et al.

Neoplasia, Journal Year: 2024, Volume and Issue: 60, P. 101102 - 101102

Published: Dec. 13, 2024

Language: Английский

Citations

0