Evidence map›Paper›PMID 35817773›Full record

ArticleNature communications2022

Blocking glycine utilization inhibits multiple myeloma progression by disrupting glutathione balance.

Jiliang Xia, Jingyu Zhang, Xuan Wu, Wanqing Du, Yinghong Zhu, Xing Liu, Zhenhao Liu, Bin Meng, Jiaojiao Guo, Qin Yang and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 72 citations in OpenAlex.

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  6. Knockdown of caspase-activated DNase and B-cell lymphoma 2 inhibits cell proliferation and drug resistance in TP53-mutant multiple myeloma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. [Progress in metabolomics of multiple myeloma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Construction of a treatment response prediction model for multiple myeloma based on multi-omics and machine learning.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  20. A prognostic model for multiple myeloma based on lipid metabolism related genes.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 5 institutions in 4 countries.

Jiliang Xia *Haihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jingyu Zhang *Haihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuan WuCancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Wanqing DuXiangya School of Public Health, Central South University, Changsha, Hunan, China.
Yinghong ZhuHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xing LiuHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhenhao LiuHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0003-4465-5925
Bin MengHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jiaojiao GuoCancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Qin YangDepartment of Hematology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yihui WangHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Qinglin WangDepartment of Laboratory Medicine, Hunan Normal University School of Medicine, Changsha, Hunan, China.
Xiangling FengXiangya School of Public Health, Central South University, Changsha, Hunan, China.
Guoxiang XieHuman Metabolomics Institute, Inc, Shenzhen, Guangdong, China.ORCID 0000-0002-0951-4150
Yi ShenDepartment of Orthopaedic Surgery, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yanjuan HeHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Juanjuan XiangCancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.ORCID 0000-0001-8712-8952
Minghua WuCancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.ORCID 0000-0001-5547-907X
Gang AnState Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin, China.
Lugui QiuState Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin, China.ORCID 0000-0002-8752-0644
Wei JiaSchool of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.ORCID 0000-0002-3739-8994
Wen ZhouHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China. wenzhou@csu.edu.cn.ORCID 0000-0003-0834-9306
Central South University · CNMinistry of Education of the People's Republic of China · CNInstitute of Hematology & Blood Diseases Hospital · CNHong Kong Baptist University · HKHunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolites in the tumor microenvironment are a critical factor for tumor progression. However, the lack of knowledge about the metabolic profile in the bone marrow (BM) microenvironment of multiple myeloma (MM) limits our understanding of MM progression. Here, we show that the glycine concentration in the BM microenvironment is elevated due to bone collagen degradation mediated by MM cell-secreted matrix metallopeptidase 13 (MMP13), while the elevated glycine level is linked to MM progression. MM cells utilize the channel protein solute carrier family 6 member 9 (SLC6A9) to absorb extrinsic glycine subsequently involved in the synthesis of glutathione (GSH) and purines. Inhibiting glycine utilization via SLC6A9 knockdown or the treatment with betaine suppresses MM cell proliferation and enhances the effects of bortezomib on MM cells. Together, we identify glycine as a key metabolic regulator of MM, unveil molecular mechanisms governing MM progression, and provide a promising therapeutic strategy for MM treatment.

Indexed as

Multiple MyelomaBone MarrowBortezomibGlutathioneGlycineHumansTumor MicroenvironmentBortezomibGlutathioneGlycine

Identifiers

PMID35817773
PMCPMC9273595
OpenAlexW4285020954

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.