Evidence map›Paper›PMID 35024200›Full record

ArticleJournal of advanced research2022

Fangchinoline diminishes STAT3 activation by stimulating oxidative stress and targeting SHP-1 protein in multiple myeloma model.

Young Yun Jung, In Jin Ha, Jae-Young Um, Gautam Sethi, Kwang Seok Ahn

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 53 citations in OpenAlex.

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  17. Skin Improvement with Antioxidant Effect of Yuja (Antioxidants (Basel, Switzerland) · 2022
    Article
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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

5 authors at 3 institutions in 2 countries.

Young Yun JungDepartment of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
In Jin HaKorean Medicine Clinical Trial Center (K-CTC), Korean Medicine Hospital, Kyung Hee University, Seoul 02447, Republic of Korea.
Jae-Young UmDepartment of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore.
Kwang Seok AhnDepartment of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
Kyung Hee University · KRDunsan Korean Medicine Hospital · KRNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The development of cancer generally occurs as a result of various deregulated molecular mechanisms affecting the genes that can control normal cellular growth. Signal transducer and activator of transcription 3 (STAT3) pathway, once aberrantly activated can promote carcinogenesis by regulating the transcription of a number of oncogenic genes. Objectives: Here, we evaluated the impact of fangchinoline (FCN) to attenuate tumor growth and survival through modulation of oncogenic STAT3 signaling pathway using diverse tumor cell lines and a xenograft mouse model. Methods: To evaluate the action of FCN on STAT3 cascade, protein levels were analyzed by Western blot analysis and electrophoretic mobility shift assay (EMSA). Translocation of STAT3 was detected by immunocytochemistry. Thereafter, FCN-induced ROS was measured by GSH/GSSG assay and H2DCF-DA. FCN-induced apoptosis was analyzed using Western blot analysis and flow cytometry for various assays. Finally, anti-cancer effects of FCN Results: We noted that FCN abrogated protein expression levels of STAT3 and upstream signals (JAK1/2 and Src). In addition, FCN also attenuated DNA binding ability of STAT3 and its translocation into the nucleus. It altered the levels of upstream signaling proteins, increased SHP-1 levels, and induced substantial apoptosis in U266 cells. FCN also promoted an increased production of reactive oxygen species (ROS) and altered GSSG/GSH ratio in tumor cells. Moreover, FCN effectively abrogated tumor progression and STAT3 activation in a preclinical myeloma model. Conclusion: Overall, this study suggests that FCN may have a tremendous potential to alter abnormal STAT3 activation and induce cell death in malignant cells along with causing the suppression of pathogenesis and growth of cancer through a pro-oxidant dependent molecular mechanism.

Indexed as

Multiple MyelomaSTAT3 Transcription FactorAnimalsBenzylisoquinolinesMiceOxidative StressProtein Tyrosine Phosphatase, Non-Receptor Type 6BenzylisoquinolinesfangchinolineProtein Tyrosine Phosphatase, Non-Receptor Type 6Ptpn6 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorApoptosisc/w, Cell per wellDAPI, 4′,6-Diamidino-2-Phenylindole, DihydrochlorideDMEM, Dulbecco’s Modified Eagle MediumFangchinolineFBS, Fetal bovine serumFCN, FangchinolineGAPDH, Glyceraldehyde 3-phosphate dehydrogenaseGSHHRP, Horseradish peroxidaseICC, ImmunocytochemistryIHC, Immunohistochemistryip, Intraperitoneal injectionJAK, Janus kinaseMMP, Matrix metalloproteinaseMultiple myelomaNT, Non treatPARP, Poly (ADP-ribose) polymeraseP/S, Penicillin-streptomycinROSRTCA, Real-time cell analysisRT-PCR, Reverse transcription polymerase chain reactionSHP-1, Src homology 2 domain-containing protein tyrosine phosphatase-1STAT3STAT3, signal transducer and activator of transcription 3VEGF, vascular endothelial growth factor

Identifiers

PMID35024200
PMCPMC8721253
OpenAlexW3137918575

What OpenQuestion holds

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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 OpenQuestion graph.