Evidence map›Paper›PMID 35387632›Full record

ArticleBMC complementary medicine and therapies2022

Hinokiflavone induces apoptosis, cell cycle arrest and autophagy in chronic myeloid leukemia cells through MAPK/NF-κB signaling pathway.

Xiang Qin, Xi Chen, Ling Guo, Jing Liu, You Yang, Yan Zeng, Cheng Li, Wenjun Liu, Wenzhe Ma

Open access · goldAbstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  7. TMJ-105, an extract ofHeliyon · 2024
    Article
  8. Article
  9. Advances in the Anti-Tumor Activity of Biflavonoids inInternational journal of molecular sciences · 2023
    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

9 authors at 2 institutions in 2 countries.

Xiang QinState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, 999078, Macau, China.
Xi ChenDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China.
Ling GuoDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China.
Jing LiuDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China.
You YangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, 999078, Macau, China.
Yan ZengDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China.
Cheng LiDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China.
Wenjun LiuDepartment of Pediatrics, The Affiliated Hospital of Southwest Medical University, Children Hematological Oncology and Birth Defects Laboratory, Sichuan Clinical Research Center for Birth Defects, No. 25, Taiping Street, Jiangyang District, Luzhou, 646000, Sichuan, China. wenjun_liu@swmu.edu.cn.
Wenzhe MaState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, 999078, Macau, China. wzma@must.edu.mo.
Affiliated Hospital of Southwest Medical University · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic myeloid leukemia (CML) is a myeloproliferative tumor originating from hematopoietic stem cells, and resistance to tyrosine kinase inhibitors (TKI) has become a major cause of treatment failure. Alternative drug therapy is one of the important ways to overcome TKI resistance. Hinokiflavone (HF) is a C-O-C type biflavonoid with low toxicity and antitumor activity. This study investigated the antitumor effect and possible mechanisms of HF in CML cells.

methodsCell viability was measured by CCK-8 assay. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Western blotting was used to assess protein expression levels.

resultsOur results showed that HF significantly inhibited the viability of K562 cells in a concentration- and time-dependent manner and induced G

conclusionHF shows a good anti-leukemia effect and is expected to become a potential therapeutic drug for CML.

Indexed as

BiflavonoidsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveApoptosisAutophagyCell Cycle CheckpointsHumansNF-kappa BSignal TransductionBiflavonoidshinokiflavoneNF-kappa BApoptosisAutophagyChronic myeloid leukemiaHinokiflavoneMAPKNF-κB

Identifiers

PMID35387632
PMCPMC8988348
OpenAlexW4223540764

What OpenQuestion holds

Textmetadata
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.