Evidence map›Paper›PMID 38460052›Full record

ArticleJournal of cancer research and clinical oncology2024

Flavokawain C inhibits proliferation and migration of liver cancer cells through FAK/PI3K/AKT signaling pathway.

Rong Wang, Rizhao Li, Huibing Yang, Xuejiao Chen, Liangliang Wu, Xiaohui Zheng, Yuepeng Jin

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

Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 7% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. 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

7 authors at 2 institutions in 1 country.

Rong WangNational Key Clinical Specialty (General Surgery), The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Rizhao LiWenzhou Medical University, Wenzhou, 325000, China.
Huibing YangWenzhou Medical University, Wenzhou, 325000, China.
Xuejiao ChenNational Key Clinical Specialty (General Surgery), The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Liangliang WuWenzhou Medical University, Wenzhou, 325000, China.
Xiaohui ZhengWenzhou Medical University, Wenzhou, 325000, China. zhengxh@wmu.edu.cn.
Yuepeng JinNational Key Clinical Specialty (General Surgery), The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. jinyuepeng@wzhospital.cn.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

National Natural Science Foundation of China 81900583the Key Laboratory of diagnosis and treatment of severe hepatopancreatic diseases of Zhejiang Province 2018E10008
6 · The paper itself

Abstract

purposeThis study investigated the potential applicability and the underlying mechanisms of flavokawain C, a natural compound derived from kava extracts, in liver cancer treatment.

methodsDrug distribution experiment used to demonstrate the preferential tissues enrichment of flavokawain C. Cell proliferation, apoptosis and migration effect of flavokawain C were determined by MTT, colony formation, EdU staining, cell adhesion, transwell, flow cytometry and western blot assay. The mechanism was explored by comet assay, immunofluorescence assay, RNA-seq-based Kyoto encyclopedia of genes and genomes analysis, molecular dynamics, bioinformatics analysis and western blot assay. The anticancer effect of flavokawain C was further confirmed by xenograft tumor model.

resultsThe studies first demonstrated the preferential enrichment of flavokawain C within liver tissues in vivo. The findings demonstrated that flavokawain C significantly inhibited proliferation and migration of liver cancer cells, induced cellular apoptosis, and triggered intense DNA damage along with strong DNA damage response. The findings from RNA-seq-based KEGG analysis, molecular dynamics, bioinformatics analysis, and western blot assay mechanistically indicated that treatment with flavokawain C notably suppressed the FAK/PI3K/AKT signaling pathway in liver cancer cells. This effect was attributed to the induction of gene changes and the binding of flavokawain C to the ATP sites of FAK and PI3K, resulting in the inhibition of their phosphorylation. Additionally, flavokawain C also displayed the strong capacity to inhibit Huh-7-derived xenograft tumor growth in mice with minimal adverse effects.

conclusionsThese findings identified that flavokawain C is a promising anticancer agent for liver cancer treatment.

Indexed as

ChalconesLiver NeoplasmsProto-Oncogene Proteins c-aktAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationFocal Adhesion Protein-Tyrosine KinasesHumansMicePhosphatidylinositol 3-KinasesSignal TransductionChalconesflavokawain CFocal Adhesion Protein-Tyrosine KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktDNA damageFAK/PI3K/AKT pathwayFlavokawain CLiver cancerMigrationProliferation

Identifiers

PMID38460052
PMCPMC10924746
OpenAlexW4392623391

What OpenQuestion holds

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LicenceCC BY
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.