Evidence map›Paper›PMID 33469314›Full record

ArticleOncoTargets and therapy2021

Aberrant SLC6A14 Expression Promotes Proliferation and Metastasis of Colorectal Cancer via Enhancing the JAK2/STAT3 Pathway.

Hongli Mao, Jinxiu Sheng, Jinlin Jia, Chang Wang, Shanfeng Zhang, Hongle Li, Fucheng He

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

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  12. Frontiers in pharmacology · 2023
    Article
  13. Review
  14. Article
  15. SLC6A14 Impacts Cystic Fibrosis Lung Disease SeverityFrontiers in molecular biosciences · 2022
    Article
  16. Article
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 at 2 institutions in 1 country.

Hongli MaoDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Jinxiu ShengDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Jinlin JiaDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Chang WangDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Shanfeng ZhangThe Laboratory Center for Basic Medicine, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Hongle LiDepartment of Molecular Pathology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Fucheng HeDepartment of Medical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.ORCID 0000-0002-9024-1144
First Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSolute carrier family 6 member 14 (SLC6A14) is a high-capacity amino acid transporter in mammalian cells. It has gained increasing attention for its potential involvement in the progression and metabolic reprogramming of various malignant tumors. However, the role of SLC6A14 in colorectal cancer (CRC) remains unclear.

methodsReal-time polymerase chain reaction (qRT-PCR), immunoblotting and immunohistochemistry were carried out to detect the expression level of SLC6A14 in human CRC tissues and CRC-derived cell lines. HCT-116 and Caco-2 cell lines were selected to conduct in vitro functional studies. Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, cell migration and invasion assays were performed to investigate the role of SLC6A14 in CRC cells. Besides, azoxymethane/dextran sulfate sodium salt (AOM/DSS)-induced CRC and tumor xenograft models were constructed to explore the effects of SLC6A14 blockade or overexpression during tumor progression in vivo.

resultsSLC6A14 was substantially increased in human CRC samples and higher levels of SLC6A14 was correlated with advanced tumor stage, lymph node metastasis and dismal survival of CRC patients. SLC6A14 markedly promoted cell growth, inhibited cell apoptosis, and exacerbated migration and invasion of CRC cells in vitro. Mechanistically, SLC6A14 aggravated these malignant phenotypes through activating JAK2/STAT3 signaling pathway, and inhibiting JAK2/STAT3 signaling with specific inhibitors could reverse SLC6A14-mediated tumorigenic effects. Besides, two different animal studies verified the tumor-promoting effect of SLC6A14 in CRC.

conclusionOur data illustrated the crucial function of SLC6A14 during CRC progression, suggesting SLC6A14/JAK2/STAT3 axis may serve as novel therapeutic targets for patients with CRC.

Indexed as

colorectal cancerCRCmigrationproliferationSLC6A14STAT3

Identifiers

PMID33469314
PMCPMC7812055
OpenAlexW3119454183

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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.