Evidence map›Paper›PMID 34007312›Full record

ArticleExperimental and therapeutic medicine2021

MTHFD2 facilitates breast cancer cell proliferation via the AKT signaling pathway.

Jun Huang, Yinyin Qin, Canfeng Lin, Xiaoguang Huang, Feiran Zhang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026
    Review
  2. Investigating the oncogenic potential of MTHFD2 in oral squamous cell carcinoma.Journal of cancer research and clinical oncology · 2026
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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

5 authors at 4 institutions in 1 country.

Jun HuangDepartment of General Thoracic Surgery, The First Affiliated Hospital of Guangzhou Medical University, Jinping, Shantou, Guangzhou 515000, P.R. China.
Yinyin QinState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Jinping, Shantou, Guangzhou 515000, P.R. China.
Canfeng LinDepartment of Oncology, Shantou Central Hospital, Jinping, Shantou, Guangzhou 515000, P.R. China.
Xiaoguang HuangDepartment of Oncology, Shantou Central Hospital, Jinping, Shantou, Guangzhou 515000, P.R. China.
Feiran ZhangDepartment of General Surgery, The First Affiliated Hospital of Shantou University Medical College, Jinping, Shantou, Guangdong 515041, P.R. China.
Shantou Central Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNShantou University · CNState Key Laboratory of Respiratory Disease · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MTHFD2 is a folate-coupled mitochondrial metabolic enzyme which has been extensively studied in breast cancer; however, its molecular functions in this cancer remain unclear. The current study aimed to reveal the underlying mechanism of breast cancer. MTHFD2 expression status and prognostic value were determined using the Gene Expression Profiling Interactive Analysis database. To determine the function of MTHFD2 in breast cancer, MCF-7 cells with stable overexpression of Flag-MTHFD2 or depletion of MTHFD2 were generated. Cell Counting Kit-8 and colony formation assays were used to examine the effect of MTHFD2 overexpression or knockout on MCF-7 cell proliferation and clonogenicity, respectively. Luciferase reporter and an AKT inhibitor (GSK6906) analysis were carried out to investigate the effect of MTHFD2 on the AKT signaling pathway. The results demonstrated that MTHFD2 expression level was higher in breast cancer tissues compared with adjacent normal tissues. Furthermore, patients with high MTHFD2 expression had significantly poorer overall survival compared with patients with low MTHFD2 expression. In addition, ectopic expression of MTHFD2 promoted the tumorigenic properties of MCF-7 cells, including proliferation and clonogenicity. Conversely, depletion of MTHFD2 had the opposite effect on the malignant properties of MCF-7 cells. Luciferase reporter demonstrated that MTHFD2 can significantly increase the ATK luciferase density. Furthermore, the Akt inhibitor GSK690693 significantly decreased the increased clonogenicity caused by MTHFD2 overexpression in MCF-7 cells. Taken together, the findings from the present study suggested that MTHFD2 may serve a protumor role in the malignancy of breast cancer by activating the AKT signaling pathway. These results provide an alternative theoretical foundation that could help the development of MTHFD2-targeted breast cancer treatment.

Indexed as

AKTbreast cancerMTHFD2proliferation

Identifiers

PMID34007312
PMCPMC8120508
OpenAlexW3159501327

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.