Evidence map›Paper›PMID 25793315›Full record

ArticleCell research2015

cMyc-mediated activation of serine biosynthesis pathway is critical for cancer progression under nutrient deprivation conditions.

Linchong Sun, Libing Song, Qianfen Wan, Gongwei Wu, Xinghua Li, Yinghui Wang, Jin Wang, Zhaoji Liu, Xiuying Zhong, Xiaoping He and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

206 citing papers in PubMed, 314 citations in OpenAlex.

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  8. PHGDH is a targetable driver of PDAC progression.bioRxiv : the preprint server for biology · 2026
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  10. RNA-binding activity of PHGDH drives amyloid-beta production in a human brain organoid model of sporadic Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  11. Review
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  15. Article
  16. Metabolic Reprogramming in Cancer Stem Cells.Cancer treatment and research · 2026
    Review
  17. Review
  18. Article
  19. Review
  20. Review

146 more citing papers are in PubMed but not listed here.

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

17 authors at 6 institutions in 1 country.

Linchong SunCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Libing SongState Key Laboratory of Oncology in Southern China and Departments of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, China.
Qianfen WanCAS Key Laboratory of Magnetic Resonance in Biological Systems, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, Hubei 430071, China.
Gongwei WuCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xinghua LiState Key Laboratory of Oncology in Southern China and Departments of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, China.
Yinghui WangCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Jin WangCAS Key Laboratory of Magnetic Resonance in Biological Systems, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, Hubei 430071, China.
Zhaoji LiuCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiuying ZhongCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiaoping HeCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Shengqi ShenCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xin PanState Key Laboratory of Proteomics, China National Center of Biomedical Analysis, Beijing 100850, China.
Ailing LiState Key Laboratory of Proteomics, China National Center of Biomedical Analysis, Beijing 100850, China.
Yulan Wang1] CAS Key Laboratory of Magnetic Resonance in Biological Systems, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, Hubei 430071, China [2] Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Ping GaoCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
Huiru Tang1] CAS Key Laboratory of Magnetic Resonance in Biological Systems, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, Hubei 430071, China [2] State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai 200433, China.
Huafeng ZhangCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Signaling Network, School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China.
University of Science and Technology of China · CNChinese Academy of Sciences · CNNational Center of Biomedical Analysis · CNSun Yat-sen University · CNSun Yat-sen University Cancer Center · CNWuhan Institute of Physics and Mathematics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells are known to undergo metabolic reprogramming to sustain survival and rapid proliferation, however, it remains to be fully elucidated how oncogenic lesions coordinate the metabolic switch under various stressed conditions. Here we show that deprivation of glucose or glutamine, two major nutrition sources for cancer cells, dramatically activated serine biosynthesis pathway (SSP) that was accompanied by elevated cMyc expression. We further identified that cMyc stimulated SSP activation by transcriptionally upregulating expression of multiple SSP enzymes. Moreover, we demonstrated that SSP activation facilitated by cMyc led to elevated glutathione (GSH) production, cell cycle progression and nucleic acid synthesis, which are essential for cell survival and proliferation especially under nutrient-deprived conditions. We further uncovered that phosphoserine phosphatase (PSPH), the final rate-limiting enzyme of the SSP pathway, is critical for cMyc-driven cancer progression both in vitro and in vivo, and importantly, aberrant expression of PSPH is highly correlated with mortality in hepatocellular carcinoma (HCC) patients, suggesting a potential causal relation between this cMyc-regulated enzyme, or SSP activation in general, and cancer development. Taken together, our results reveal that aberrant expression of cMyc leads to the enhanced SSP activation, an essential part of metabolic switch, to facilitate cancer progression under nutrient-deprived conditions.

Indexed as

AnimalsApoptosisCarcinoma, HepatocellularCell ProliferationFood DeprivationGene Expression Regulation, NeoplasticGlutathioneHumansLiver NeoplasmsMetabolic Networks and PathwaysMicePhosphoric Monoester HydrolasesProto-Oncogene Proteins c-mycSerineTransaminasesGlutathionePhosphoric Monoester Hydrolasesphosphoserine aminotransferasephosphoserine phosphataseProto-Oncogene Proteins c-mycSerineTransaminases

Identifiers

PMID25793315
PMCPMC4387561
OpenAlexW1987798277

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.