Literature DB >> 35430564

Deletion of MTAP Highly Sensitizes Osteosarcoma Cells to Methionine Restriction With Recombinant Methioninase.

Yusuke Aoki1,2,3, Yasunori Tome4, Qinghong Han1, Jun Yamamoto1,2, Kazuyuki Hamada1,2, Noriyuki Masaki1,2, Yutaro Kubota1,2, Michael Bouvet2, Kotaro Nishida3, Robert M Hoffman5,2.   

Abstract

BACKGROUND/AIM: Methionine addiction is a fundamental and general hallmark of cancer cells, which require exogenous methionine, despite large amounts of methionine synthesized endogenously. 5-Methylthioadenosine phosphorylase (MTAP) plays a principal role as an enzyme in the methionine-salvage pathway, which produces methionine and adenine from methylthioadenosine and is deleted in 27.5% to 37.5% of osteosarcoma patients.
MATERIALS AND METHODS: Human osteosarcoma cell lines U2OS, SaOS2, MNNG/HOS (HOS) and 143B, were used. The MTAP gene was knocked out in U2OS with CRISPR/Cas9. 143B and HOS have an MTAP deletion and SaOS2 is positive for MTAP. MTAP was determined by western blotting. The four cell lines were compared for sensitivity to recombinant methioninase (rMETase).
RESULTS: MTAP-deleted osteosarcoma cell lines MNNG/HOS and 143B were significantly more sensitive to rMETase than MTAP-positive osteosarcoma cell lines U2OS and SaOS2. In addition, MTAP knock-out U2OS cells were more sensitive to rMETase than the parental MTAP-positive U2OS cells.
CONCLUSION: The present results demonstrated that the absence of MTAP sensitizes osteosarcoma cells to methionine restriction by rMETase, a promising clinical strategy. Copyright
© 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Entities:  

Keywords:  CRISPR/Cas9; Hoffman efffect; MTAP; Osteosarcoma; deletion; knockout; methionine addiction; methionine restriction; recombinant methioninase

Mesh:

Substances:

Year:  2022        PMID: 35430564      PMCID: PMC9016482          DOI: 10.21873/cgp.20321

Source DB:  PubMed          Journal:  Cancer Genomics Proteomics        ISSN: 1109-6535            Impact factor:   4.069


  37 in total

1.  Broad selective efficacy of recombinant methioninase and polyethylene glycol-modified recombinant methioninase on cancer cells In Vitro.

Authors:  Yuying Tan; Mingxu Xu; Robert M Hoffman
Journal:  Anticancer Res       Date:  2010-04       Impact factor: 2.480

2.  MAT2A Inhibition Blocks the Growth of MTAP-Deleted Cancer Cells by Reducing PRMT5-Dependent mRNA Splicing and Inducing DNA Damage.

Authors:  Peter Kalev; Marc L Hyer; Stefan Gross; Zenon Konteatis; Chi-Chao Chen; Mark Fletcher; Max Lein; Elia Aguado-Fraile; Victoria Frank; Amelia Barnett; Everton Mandley; Joshua Goldford; Yue Chen; Katie Sellers; Sebastian Hayes; Kate Lizotte; Phong Quang; Yesim Tuncay; Michelle Clasquin; Rachel Peters; Jaclyn Weier; Eric Simone; Joshua Murtie; Wei Liu; Raj Nagaraja; Lenny Dang; Zhihua Sui; Scott A Biller; Jeremy Travins; Kevin M Marks; Katya Marjon
Journal:  Cancer Cell       Date:  2021-01-14       Impact factor: 31.743

3.  Methylthioadenosine phosphorylase, a gene frequently codeleted with p16(cdkN2a/ARF), acts as a tumor suppressor in a breast cancer cell line.

Authors:  Scott A Christopher; Paula Diegelman; Carl W Porter; Warren D Kruger
Journal:  Cancer Res       Date:  2002-11-15       Impact factor: 12.701

4.  Defects in methylthioadenosine phosphorylase are associated with but not responsible for methionine-dependent tumor cell growth.

Authors:  B Tang; Y N Li; W D Kruger
Journal:  Cancer Res       Date:  2000-10-01       Impact factor: 12.701

5.  Methylthioadenosine phosphorylase gene deletions are common in osteosarcoma.

Authors:  José M García-Castellano; Alberto Villanueva; John H Healey; Rebecca Sowers; Carlos Cordon-Cardo; Andrew Huvos; Joseph R Bertino; Paul Meyers; Richard Gorlick
Journal:  Clin Cancer Res       Date:  2002-03       Impact factor: 12.531

6.  MTAP Deletions in Cancer Create Vulnerability to Targeting of the MAT2A/PRMT5/RIOK1 Axis.

Authors:  Katya Marjon; Michael J Cameron; Phong Quang; Michelle F Clasquin; Everton Mandley; Kaiko Kunii; Michael McVay; Sung Choe; Andrew Kernytsky; Stefan Gross; Zenon Konteatis; Joshua Murtie; Michelle L Blake; Jeremy Travins; Marion Dorsch; Scott A Biller; Kevin M Marks
Journal:  Cell Rep       Date:  2016-04-07       Impact factor: 9.423

7.  Methylthioadenosine phosphorylase deficiency in Japanese osteosarcoma patients.

Authors:  Shinichi Miyazaki; Junji Nishioka; Taizou Shiraishi; Akihiko Matsumine; Atsumasa Uchida; Tsutomu Nobori
Journal:  Int J Oncol       Date:  2007-11       Impact factor: 5.650

8.  Enhanced in vitro selective toxicity of chemotherapeutic agents for human cancer cells based on a metabolic defect.

Authors:  P H Stern; R M Hoffman
Journal:  J Natl Cancer Inst       Date:  1986-04       Impact factor: 13.506

9.  Over-methylation of Histone H3 Lysines Is a Common Molecular Change Among the Three Major Types of Soft-tissue Sarcoma in Patient-derived Xenograft (PDX) Mouse Models.

Authors:  Yusuke Aoki; Jun Yamamoto; Yasunori Tome; Kazuyuki Hamada; Noriyuki Masaki; Sachiko Inubushi; Yoshihiko Tashiro; Michael Bouvet; Itaru Endo; Kotaro Nishida; Robert M Hoffman
Journal:  Cancer Genomics Proteomics       Date:  2021 Nov-Dec       Impact factor: 4.069

10.  Nutrient availability shapes methionine metabolism in p16/MTAP-deleted cells.

Authors:  Sydney M Sanderson; Peter G Mikhael; Vijyendra Ramesh; Ziwei Dai; Jason W Locasale
Journal:  Sci Adv       Date:  2019-06-26       Impact factor: 14.136

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