Targeting GLS1 to cancer therapy through glutamine metabolism.

Wei Yu, XiangYu Yang, Qian Zhang, Li Sun, ShengTao Yuan, YongJie Xin

Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 2022;23(11):2253-2268

PMID: 34023970

Full Text on Springer View on PubMed

Abstract

Glutamine metabolism is one of the hallmarks of cancers which is described as an essential role in serving as a major energy and building blocks supply to cell proliferation in cancer cells. Many malignant tumor cells always display glutamine addiction. The "kidney-type" glutaminase (GLS1) is a metabolism enzyme which plays a significant part in glutaminolysis. Interestingly, GLS1 is often overexpressed in highly proliferative cancer cells to fulfill enhanced glutamine demand. So far, GLS1 has been proved to be a significant target during the carcinogenesis process, and emerging evidence reveals that its inhibitors could provide a benefit strategy for cancer therapy. Herein, we summarize the prognostic value of GLS1 in multiple cancer type and its related regulatory factors which are associated with antitumor activity. Moreover, this review article highlights the remarkable reform of discovery and development for GLS1 inhibitors. On the basis of case studies, our perspectives for targeting GLS1 and development of GLS1 antagonist are discussed in the final part.

Address: China Pharmaceutical University, Nanjing, 21000, Jiangsu, China.; Zhuhai Interventional Medical Center, Zhuhai Precision Medical Center, Zhuhai People's Hospital, Zhuhai Hospital Affiliated With Jinan University, Jinan University, Zhuhai, 519000, Guangdong, China.; China Pharmaceutical University, Nanjing, 21000, Jiangsu, China. [email protected].; Zhuhai Interventional Medical Center, Zhuhai Precision Medical Center, Zhuhai People's Hospital, Zhuhai Hospital Affiliated With Jinan University, Jinan University, Zhuhai, 519000, Guangdong, China. [email protected].

DOI: 10.1007/s12094-021-02645-2

Link outs

Free resources

Medical:

https://medlineplus.gov/cancer.html

Other Literature Sources:

https://scite.ai/reports/34023970

Miscellaneous:

https://assays.cancer.gov/CPTAC-516

Subscription / membership required

Full Text Sources:

https://dx.doi.org/10.1007/s12094-021-02645-2

MeSH Terms: Apoptosis, Benzophenanthridines, Cell Proliferation, Diazooxonorleucine, Disease Progression, Drug Resistance, Neoplasm, Genes, myc, Glutaminase, Glutamine, Humans, MicroRNAs, NF-kappa B, Neoplasm Proteins, Neoplasms, Oxidation-Reduction, Phosphates, Prognosis, Retinoblastoma Protein, Sulfides, Thiadiazoles