Evidence map›Paper›PMID 39696051›Full record

ArticleBMC cancer2024

Redox homeostasis of one-carbon metabolism-dependent reprogramming is critical for RCC progression under exogenous serine/glycine-deprived conditions.

Huijuan Wang, Mengzhen Fan, Sichang Liu, Mengjiao Qu, Xin Hou, Junqing Hou, Yanxin Xu, Xiaodi Shang, Chen Liu, Mingxia He and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
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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

13 authors.

Huijuan Wang *Joint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Mengzhen Fan *Joint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Sichang Liu *Joint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Mengjiao Qu *Joint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Xin HouThe First Affiliated Hospital of Henan University, Henan University, Kaifeng, China.
Junqing HouKaifeng 155 Hospital, RongTong Medical Healthcare Group Co. Ltd, Kaifeng, China.
Yanxin XuJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Xiaodi ShangStem Cells and Biotherapy Engineering Research Center of Henan, National Joint Engineering Laboratory of Stem Cells and Biotherapy, School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, China.
Chen LiuJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Mingxia HeJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Jianzheng GaoJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China.
Jingying ChenJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China. chenjy135@163.com.
Xia LiJoint National Laboratory for Antibody Drug Engineering, School of Medicine, Henan University, Kaifeng, 475004, China. lixia_kf@126.com.

Funding

Kaifeng Science and Technology Plan Project 2303006National Natural Science Foundation of China U22A20382, 32270977Science and Technology Department, Henan Province 222102310609
6 · The paper itself

Abstract

backgroundSerine/glycine are critical for the growth and survival of cancer cells. Some cancer cells are more dependent on exogenous serine/glycine than endogenously synthesized serine/glycine. However, the function and underlying mechanisms of exogenous serine/glycine in renal cell carcinoma (RCC) remain unclear.

methodsWe conducted a comprehensive assessment of RCC progression under conditions of exogenous serine/glycine deprivation and explored the underlying mechanism via immunofluorescence, autophagic flux analysis, extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) measurements.

resultsThe expression of the serine synthesis pathway enzymes was decreased in RCC specimens, the de novo serine synthesis pathway (SSP) was reduced in RCC. And the levels of endogenously synthesized serine/glycine were little. Yet, the exogenous serine/glycine deprivation significantly inhibited the growth of RCC cells both in vitro and in vivo, indicating that exogenous serine/glycine were important for RCC progression. Mechanistically, the deprivation of exogenous serine/glycine disrupted one-carbon metabolism and increased the ratio of NAD(P)

conclusionsOur results indicate that exogenous serine/glycine are critical for RCC progression by maintaining one-carbon metabolism-dependent redox homeostasis, which provides new insights for the development of dietary serine/glycine starvation-based therapeutic approaches for RCC.

Indexed as

AutophagyCarbonCarcinoma, Renal CellDisease ProgressionGlycineHomeostasisKidney NeoplasmsOxidation-ReductionSerineAnimalsCell Line, TumorCell ProliferationFemaleHumansLysosomesMaleCarbonGlycineReactive Oxygen SpeciesSerineLysosomal dependent cell deathLysosome membrane permeabilizationRenal cell carcinomaROSSerine/glycine

Identifiers

PMID39696051
PMCPMC11658248

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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.