Evidence map›Paper›PMID 34398363›Full record

ArticleEsophagus : official journal of the Japan Esophageal Society2022

In vitro anti-cancer effect of marmesin by suppression of PI3K/Akt pathway in esophagus cancer cells.

Qi Wang, Sheng Zhong, Hua Wu, Qingquan Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Esophagus : official journal of the Japan Esophageal Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Article
  3. Solute carrier family 16 member 3 is a target of nodakenetin in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  4. Exploring Natural Coumarins: Breakthroughs in Anticancer Therapeutics.Anti-cancer agents in medicinal chemistry · 2026
    Review
  5. Article
  6. Medicinal Potential ofPlants (Basel, Switzerland) · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The GenusMolecules (Basel, Switzerland) · 2022
    Review
  13. Article
  14. 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

4 authors at 2 institutions in 1 country.

Qi WangDepartment of Thoracic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huan'an, 223000, China.
Sheng ZhongDepartment of Thoracic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huan'an, 223000, China.
Hua WuDepartment of Thoracic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huan'an, 223000, China.
Qingquan WuDepartment of Thoracic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huan'an, 223000, China. wuqingquan8888@163.com.
Huaian First People’s Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMarmesin, an important coumarin isolated from Broussonetia kazinoki, has been proposed to possess many pharmacological activities including anti-tumor activity. However, the anti-cancer effect of marmesin on esophageal cancer (EC) has not been characterized. The study aimed to explore the anti-cancer role of marmesin using EC cell lines in vitro. METHODS AND

resultsCell proliferation was evaluated by CCK-8 and Edu cell proliferation assays and apoptosis was detected by TUNEL assay. Western blot analysis was used to determine the expression of Ki67, proliferating cell nuclear antigen (PCNA), Bcl-2, Bax, phosphatidylinositol 3-kinase (PI3K), phosphoryrated-PI3K (p-PI3K), protein kinase B (Akt), and phosphoryrated-Akt (p-Akt). The mechanism of action of marmesin was analyzed using network pharmacology approach. Marmesin exhibited anti-proliferative effect against EC cells, which was further confirmed by the reduced expression of Ki67 and PCNA. Marmesin exerted pro-apoptotic activity on EC cells by downregulating Bcl-2 and upregulating Bax. According to the results from network pharmacology approach, we speculated that PI3K/Akt pathway may participate in the effect of marmesin on EC cells. Additionally, the PI3K/Akt pathway was suppressed by marmesin in EC cells. Moreover, forced expression of Akt reversed the inhibition of cell proliferation and induction of apoptosis induced by marmesin in EC cells.

conclusionsMarmesin exerted anti-cancer activity in EC cells by inhibiting the PI3K/Akt pathway.

Indexed as

Esophageal NeoplasmsPhosphatidylinositol 3-KinaseCell Line, TumorCoumarinsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCoumarinsmarmesinPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisEsophageal cancerMarmesinNetwork pharmacologyPI3K/Akt pathwayProliferation

Identifiers

PMID34398363
OpenAlexW3196274060

What Socratic holds

Textmetadata
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.