Evidence map›Paper›PMID 34036398›Full record

ArticleOncology reports2021

Phlorizin from sweet tea inhibits the progress of esophageal cancer by antagonizing the JAK2/STAT3 signaling pathway.

Zhenxian Jia, Yuning Xie, Hongjiao Wu, Zhuo Wang, Ang Li, Ze Li, Zhenbang Yang, Zhi Zhang, Zhaobin Xing, Xuemei Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 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
1.4field-weighted citation impact, top 19% 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, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Anticancer Potential of Natural Chalcones: In Vitro and In Vivo Evidence.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Autophagy in gastrointestinal cancers.Frontiers in oncology · 2022
    Review
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

10 authors at 2 institutions in 1 country.

Zhenxian JiaSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Yuning XieSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Hongjiao WuCollege of Life Science, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Zhuo WangSchool of Pharmacy, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Ang LiSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Ze LiSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Zhenbang YangSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Zhi ZhangDepartment of Oncology, Affiliated Tangshan Gongren Hospital, North China University of Science and Technology, Tangshan, Hebei 063000, P.R. China.
Zhaobin XingCollege of Life Science, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
Xuemei ZhangSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
North China University of Science and Technology · CNTangshan Gongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phlorizin, an important member of the dihydrochalcone family, has been widely used as a Chinese Traditional Medicine for treatment of numerous diseases. The present study aimed to investigate the potential therapeutic effects of phlorizin on esophageal cancer. Phlorizin, extracted from sweet tea, was used to treat esophageal cancer cells. Cell proliferation, migration and invasion were determined using Cell Counting Kit‑8 and colony formation assays, and wound healing and Transwell assays, respectively. RNA sequencing and bioinformatics analysis was used to investigate the potential mechanism of phlorizin in the development of esophageal cancer. Fluorescent staining and flow cytometry was used to measure the level of apoptosis. The expression level of the proteins, P62/SQSTM1 and LC3 І/II, and the effect of phlorizin on the JAK2/STAT3 signaling pathway was detected using western blot analysis. The results demonstrated that phlorizin could inhibit cell proliferation, migration and invasion. Bioinformatics analysis showed that phlorizin might be involved in pleiotropic effects, such as the 'JAK/STAT signaling pathway' (hsa04630), 'MAPK signaling pathway'(hsa04010) and 'apoptosis' (hsa04210). It was also confirmed that phlorizin promoted apoptosis and inhibited autophagy in the esophageal cancer cells. Notably, phlorizin might inhibit the proteins in the JAK/STAT signaling pathway, which would affect cancer cells. Taken together, the present data showed that phlorizin inhibited the progression of esophageal cancer by antagonizing the JAK2/STAT3 signaling pathway.

Indexed as

AutophagyCamellia sinensisCell Line, TumorCell MovementCell ProliferationCell SurvivalEsophageal NeoplasmsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansJanus Kinase 2PhlorhizinPlant ExtractsSequence Analysis, RNASignal TransductionSTAT3 Transcription FactorJAK2 protein, humanJanus Kinase 2PhlorhizinPlant ExtractsSTAT3 Transcription Factoresophageal cancerJAK2phlorizinSTAT3sweet tea

Identifiers

PMID34036398
PMCPMC8165578
OpenAlexW3162767843

What Socratic 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 Socratic graph.