The identification and structural characterization of C7orf24 as γ-glutamyl cyclotransferase. An essential enzyme in the γ-glutamyl cycle. VOLUME 283 (2008) PAGES 22031-22042

Oakley, A.J.; Yamada, Tetsuo; Liú, Dan; Coggan, Marjorie; Clark, Andy; Board, Philip G.

doi:10.1016/s0021-9258(20)56958-5

Cited by 4 publications

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“…The role of CHAC2 in the GSH metabolism cycle is clear [23]. To further examine the influence of CHAC2 on the progression of lung adenocarcinoma, we explored the expression profile of CHAC2 using public databases.…”

Section: Discussionmentioning

confidence: 99%

CHAC2 promotes lung adenocarcinoma by regulating ROS-mediated MAPK pathway activation

Peng¹,

Wen²,

Jiang³

et al. 2023

J. Cancer

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An imbalance in ROS (reactive oxidative species) and the antioxidant barrier regulates the process of tumorigenesis. GSH has a key effect in preventing cells from oxidative damage by scavenging ROS. The role of CHAC2, an enzyme regulating GSH, in lung adenocarcinoma remains unknown. Here, RNA sequencing data analysis and immunohistochemistry (IHC) assays of lung adenocarcinoma and normal lung tissues were used to verify the expression of CHAC2. The effect of CHAC2 on the proliferation abilities of lung adenocarcinoma cells was examined using a series of overexpression or knockout assays. RNA sequencing and IHC results showed that the expression level of CHAC2 in lung adenocarcinoma was higher than that in normal lung tissues. CCK-8, colony formation and subcutaneous xenograft experiments in BALB/c nude mice showed that in vitro and in vivo CHAC2 promoted the growth capacity of lung adenocarcinoma cells. Subsequent immunoblot, immunohistochemistry and flow cytometry experiments showed that CHAC2 increased ROS by reducing GSH in lung adenocarcinoma and that the elevated ROS activated the MAPK pathway. Our investigation identified a new role for CHAC2 and elucidated the mechanism by which CHAC2 promotes lung adenocarcinoma progression.

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Section: Discussionmentioning

confidence: 99%

CHAC2 promotes lung adenocarcinoma by regulating ROS-mediated MAPK pathway activation

Peng¹,

Wen²,

Jiang³

et al. 2023

J. Cancer

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“…PSME1 belongs to PA28 γ Proteasome subunit, recent studies have proved that PSME1 plays a role in the transformation and progress of MM cells (30). GGCT can catalyze the formation of 5oxoproline from gamma-glutamyl dipeptides and participate in glutathione homeostasis (41). GGCT promotes the metastasis and invasion of colon cancer through the transformation of epidermal stromal cells (42).…”

Section: Discussionmentioning

confidence: 99%

A gene expression signature based on cell-death related gene expression in multiple myeloma

Zhu,

Deng,

et al. 2023

Preprint

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Background Multiple myeloma (MM) is a complex hematological malignancy characterized by the uncontrolled monoclonal expansion of malignant plasma cells within the bone marrow. The identification of reliable prognostic biomarkers is paramount in the precise risk stratification of MM patients and the tailoring of personalized therapeutic interventions. Methods This comprehensive study harnessed gene expression profiles and clinical data obtained from a cohort of 2080 Multiple myeloma patients drawn from five distinct datasets. These resources were leveraged to construct a prognostic model centered around the intricate phenomenon of cell death. We meticulously integrated microarray gene expression data from the GEO database and the MMRF-CoMMpass dataset sourced from the TCGA website. Our approach for formulating the cell death signature encompassed genes associated with a diverse array of cell death mechanisms, including apoptosis, autophagy, pyroptosis, and necroptosis. Utilizing Lasso regression, we meticulously selected variables and assigned weights, ultimately culminating in the selection of 40 genes for the development of the cell death risk score model. In addition, we conducted a thorough gene set enrichment analysis to probe the biological pathways that underwent aberrant activation within the high-risk patient cohort. Results Our cell death prognosis model exhibited exceptional proficiency in predicting overall survival. When integrated with the International Staging System (ISS), our model further refined the precision of prognosis prediction. Furthermore, our gene set enrichment analysis unveiled the abnormal activation of multiple pivotal biological pathways within the high-risk patient subset. Conclusion The prognosis model founded upon cell death-associated genes not only offers outstanding predictive performance but also facilitates the enhanced identification of high-risk MM patients. It stands as a robust tool for customizing treatment strategies and refining risk stratification. This groundbreaking research holds substantial promise in advancing our understanding of MM pathogenesis, thereby bolstering the development of more efficacious therapeutic approaches.

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“…It is the most abundant antioxidant in vivo and has multiple functions; however, in cancers, excessive elevation of GSH promotes tumor progression 12 . GGCT, γ-glutamylcyclotransferase, originally named as C7orf24, is an enzyme involved in the γ-glutamyl cycle that is essential for GSH homeostasis, and is known for its oncogenicity and utility as a tumor marker 13,14 . It is thought that the first detection of elevated GGCT in tumors was a study comparing bladder urothelial carcinomas and normal controls 15 , followed by reports of elevated levels in breast, ovarian, cervical, lung, colon, and esophageal squamous cell carcinomas, glioma, and OS 16 .…”

Section: Introductionmentioning

confidence: 99%

Myc upregulates Ggct, γ-glutamylcyclotransferase to promote development ofp53-deficient osteosarcoma

Ueno,

Otani,

Date

et al. 2024

Preprint

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Osteosarcoma (OS) in humans is characterized by alterations in theTP53gene. In mice, loss of p53 triggers OS development, for which c-Myc (Myc) oncogenicity is indispensable. However, little is known about which genes are targeted by Myc to promote tumorigenesis. Here, we examined the role of Ggct, γ-glutamylcyclotransferase which is a component enzyme of γ-glutamyl cycle essential for glutathione homeostasis, in human and mouse OS development. We found thatGGCTis a poor prognostic factor for human OS, and that deletion ofGgctsuppressesp53-deficient osteosarcomagenesis in mice. Myc upregulates Ggct directly by binding to theGgctpromoter, and deletion of a Myc binding site therein by genome editing attenuated the tumorigenic potential ofp53-deficient OS cells. Taken together, these results show a rationale that GGCT is widely upregulated in cancer cells and solidify its suitability as a target for anticancer drugs.

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The identification and structural characterization of C7orf24 as γ-glutamyl cyclotransferase. An essential enzyme in the γ-glutamyl cycle. VOLUME 283 (2008) PAGES 22031-22042

Cited by 4 publications

References 0 publications

CHAC2 promotes lung adenocarcinoma by regulating ROS-mediated MAPK pathway activation

CHAC2 promotes lung adenocarcinoma by regulating ROS-mediated MAPK pathway activation

A gene expression signature based on cell-death related gene expression in multiple myeloma

Myc upregulates Ggct, γ-glutamylcyclotransferase to promote development ofp53-deficient osteosarcoma

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