Evidence map›Paper›PMID 35184647›Full record

ArticleBioengineered2022

Eriodictyol suppresses the malignant progression of colorectal cancer by downregulating tissue specific transplantation antigen P35B (TSTA3) expression to restrain fucosylation.

Hua Huang, Yun He, Youran Li, Mingjia Gu, Minna Wu, Lijiang Ji

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. 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
1.8field-weighted citation impact, top 15% 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, 23 citations in OpenAlex.

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  16. International journal of molecular sciences · 2022
    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

6 authors at 1 institution in 1 country.

Hua HuangDepartment of Anorectal, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Changshu, Jiangsu Province, China.
Yun HeDepartment of Oncology, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Changshu, Jiangsu Province, China.
Youran LiDepartment of Anorectal, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China.
Mingjia GuDepartment of Nephrology, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Changshu, Jiangsu Province, China.
Minna WuDepartment of Anorectal, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China.
Lijiang JiDepartment of Anorectal, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine, Changshu, Jiangsu Province, China.
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eriodictyol is a natural flavonoid with many pharmacological effects, such as anti-oxidation, anti-inflammation, anti-tumor, and neuroprotection. Besides, it has been reported that flavonoids play an important role in protein glycosylation. The fucosylation structure is closely associated with processes of various tumor metastases. TSTA3 is involved in the de novo synthesis and can convert cellular GDP-D-mannose into GDP-L-fucose. It was predicted on the STITCH database that eriodictyol interacted with TSTA3. In addition, literature has confirmed that TSTA3 is upregulated in CRC and can regulate the proliferation and migration of breast cancer cells. Herein, the precise effects of eriodictyol on the clone-forming, proliferative, migratory and invasive abilities of CRC cells as well as EMT process were assessed. Moreover, the correlation among eriodictyol, TSTA3, and fucosylation in these malignant behaviors of CRC cells was evaluated, in order to elucidate the underlying mechanism. The current work discovered that eriodictyol inhibited the viability, clone-formation, proliferation, migration, invasion, and EMT of CRC cells, and that these inhibitory effects of eriodictyol on the malignant behavior of CRC cells were reversed by TSTA3 overexpression. Additionally, eriodictyol suppresses fucosylation by downregulating the TSTA3 expression. Results confirmed that fucosylation inhibitor (2-F-Fuc) inhibited clone formation, proliferation, migration, invasion, as well as EMT of CRC cells and eriodictyol treatment further reinforced the suppressing effects of 2-F-Fuc on the malignant behavior of CRC cells. We conclude that eriodictyol suppresses the clone-forming, proliferative, migrative and invasive abilities of CRC cells as well as represses the EMT process by downregulating TSTA3 expression to restrain fucosylation.

Indexed as

Carbohydrate EpimerasesColorectal NeoplasmsKetone OxidoreductasesCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFlavanonesGlycosylationGuanosine Diphosphate FucoseHumansCarbohydrate EpimeraseseriodictyolFlavanonesGuanosine Diphosphate FucoseKetone OxidoreductasesTSTA3 protein, humancolorectal cancerEriodictyolfucosylationTSTA3

Identifiers

PMID35184647
PMCPMC8973719
OpenAlexW4213314033

What OpenQuestion holds

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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.