Evidence map›Paper›PMID 39578351›Full record

ArticleCancer control : journal of the Moffitt Cancer Center

Anti-Tumor Effect and Mechanism Study of Caloric Restriction, Achieved by Time-Restricted Feeding, in Mice.

Weisheng Lu, Jue Wang, Chengji Wang, Haijie Wang, Wenhao Gao, Shouchong Ye, Ruling Shen

Abstract read
In one paragraph

Article in Cancer control : journal of the Moffitt Cancer Center. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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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

7 authors.

Weisheng LuModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.ORCID 0009-0006-8915-324X
Jue WangModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.
Chengji WangModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.
Haijie WangModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.
Wenhao GaoModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.
Shouchong YeModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.
Ruling ShenModel Organism Research and Development Department, Shanghai Laboratory Animal Research Center, Shanghai, China.ORCID 0000-0002-7529-810X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo evaluate the therapeutic effects and explore the mechanisms behind caloric restriction achieved through time-restricted feeding (CR) in inhibiting mouse tumors, providing a theoretical basis and data support for future CR diet-assisted anticancer treatment protocols.

methodsC57BL/6 and BALB/c mice were divided into four cell line groups. Each group was further split into normal diet (ND) and a CR diet groups. The ND groups had free access to water and a normal diet, while the CR diet groups had access to water but were only fed from 9 a.m. to 11 a.m., fasting for the remaining 22 h. Food intake was recorded daily starting on day 1 of the experiment. Tumor models were established and assessed every 2 days. Blood biochemical indicators, serum pyruvic acid levels, and cytokine expression were measured.

resultsThe CR diet inhibited tumor growth in mice. Colorimetric assays and ELISAs showed a reduction in pyruvic acid levels and in key upstream and downstream rate-limiting enzymes in the sera of CR mice. Routine blood and blood biochemistry tests suggested minor effects of the CR diet on these parameters. Western blotting revealed that the CR diet suppressed mTOR and AKT protein expression in tumor tissues. ELISA showed that various mTOR-related signaling pathways were downregulated. Immunohistochemistry staining indicated reduced expression of P53, P-AKT, EGFR, and IGF-1 in tumor tissues. TUNEL staining confirmed that the CR diet promoted tumor apoptosis.

conclusionThe CR diet inhibited tumor growth by suppressing mTOR and its related upstream and downstream gene signaling pathways, reducing tumor glycolysis, and accelerating tumor cell apoptosis.

Indexed as

Caloric RestrictionAnimalsApoptosisCell Line, TumorCell ProliferationHumansMiceMice, Inbred BALB CMice, Inbred C57BLSignal TransductionTOR Serine-Threonine KinasesTOR Serine-Threonine Kinasesapoptosiscaloric-restrictedMammalian target of rapamycinphosphorylated protein kinase Btumor glycolysistumor inhibition

Identifiers

PMID39578351
PMCPMC11585051

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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.