Evidence map›Paper›PMID 39571599›Full record

ArticleCancer medicine2024

MTHFD1 Regulates Autophagy to Promote Growth and Metastasis in Colorectal Cancer via the PI3K-AKT-mTOR Signaling Pathway.

Zhihao Li, Haoxian Ke, Jiawei Cai, Shubiao Ye, Junfeng Huang, Chi Zhang, Ming Yuan, Ping Lan, Xianrui Wu

Abstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
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  4. Frontiers in immunology · 2026
    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

9 authors.

Zhihao LiDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0003-3465-7994
Haoxian KeDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Jiawei CaiDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Shubiao YeDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Junfeng HuangDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Chi ZhangDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Ming YuanDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0003-2935-3320
Ping LanDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0002-5225-5027
Xianrui WuDepartment of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0002-4743-7133

Funding

Fundamental Research Funds for the Central Universities, Sun Yat-sen University 23xkjc023Key Research and Development Program of Guangzhou City SL2024B03J00078National Key Research and Development Program of China 2022YFA1304000National Natural Science Foundation of China Key Joint Project U21A20344open project of BGI-Shenzhen, Shenzhen 518000, China BGIRSZ20220008open project of Guangdong Provincial Key Laboratory of Human Disease Genomics 2020B1212070028Science and Technology Program of Shenzhen, China JCYJ20190807161807867the National Natural Science Foundation of China 81970452the National Natural Science Foundation of China 82370675the program of the Guangdong Provincial Clinical Research Center for Digestive Diseases 2020B1111170004
6 · The paper itself

Abstract

objectivesMethylenetetrahydrofolate dehydrogenase 1 (MTHFD1) is the enzyme with the activities of methylenetetrahydrofolate dehydrogenase, methylenetetrahydrofolate cyclohydrolase, and formyltetrahydrofolate synthetase. Our aim was to elucidate the function of MTHFD1 in colorectal cancer (CRC).

methodsIn vitro assessments of the proliferation, invasion, and migration abilities of CRC cells were conducted using Immunohistochemistry, Transwell invasion assays, Western blot (WB), and Cell counting Kit-8 assays. WB was also utilized to measure autophagy protein levels and PI3K-AKT-mTOR signaling pathway expression. Furthermore, the role of MTHFD1 was evaluated in vivo by using subcutaneous xenograft tumor models and lateral tail vein metastasis models of human CRC in nude mice.

resultsOverexpression of MTHFD1 promoted the abilities of tumorigenesis and metastasis in CRC in vitro and in vivo and reduced autophagy, attributing to the PI3K-AKT-mTOR signaling pathway in CRC cells. In contrast, the down-regulation of MTHFD1 increased autophagy and suppressed their proliferation, migration, and invasion.

conclusionsMTHFD1 can modulate the PI3K-AKT-mTOR signaling pathway to suppress autophagy and stimulate tumorigenesis and metastasis.

Indexed as

AutophagyCell MovementCell ProliferationColorectal NeoplasmsMethylenetetrahydrofolate Dehydrogenase (NADP)Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMethylenetetrahydrofolate Dehydrogenase (NADP)Minor Histocompatibility AntigensMTHFD1 protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesautophagycolorectal cancerinvasionmigrationMTHFD1PI3K‐AKT‐mTORproliferation

Identifiers

PMID39571599
PMCPMC11581708

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.