Evidence map›Paper›PMID 31575007›Full record

ArticleBiomolecules2019

Brusatol, a Nrf2 Inhibitor Targets STAT3 Signaling Cascade in Head and Neck Squamous Cell Carcinoma.

Jong Hyun Lee, Shobith Rangappa, Chakrabhavi Dhananjaya Mohan, Basappa, Gautam Sethi, Zhi-Xiu Lin, Kanchugarakoppal S Rangappa, Kwang Seok Ahn

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 80 citations in OpenAlex.

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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

8 authors at 5 institutions in 5 countries.

Jong Hyun LeeCollege of Korean Medicine, Kyung Hee University, #47, Kyungheedae-gil, Dongdaemoon-gu, Seoul 130-701, Korea. 88mirue@gmail.com.
Shobith RangappaAdichunchanagiri Institute for Molecular Medicine, BG Nagara-571448, Nagamangala Taluk, Mandya District 571448, India. shobithrangappa@gmail.com.
Chakrabhavi Dhananjaya MohanDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysore 570006, India. cd.mohan@yahoo.com.
BasappaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, India. salundibasappa@gmail.com.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore. phcgs@nus.edu.sg.
Zhi-Xiu LinFaculty of Medicine, The Chinese University of Hong Kong, Rm 101, 1/F Li Wai Chun Building, CUHK, Shatin, N.T. 999077, Hong Kong. linzx@cuhk.edu.hk.
Kanchugarakoppal S RangappaInstitution of Excellence, Vijnana Bhavan, University of Mysore, Manasagangotri, Mysore 570006, India. rangappaks@yahoo.com.
Kwang Seok AhnCollege of Korean Medicine, Kyung Hee University, #47, Kyungheedae-gil, Dongdaemoon-gu, Seoul 130-701, Korea. ksahn@khu.ac.kr.ORCID 0000-0002-2882-0612
University of Mysore · INKyung Hee University · KRChinese University of Hong Kong · HKInstitute for Molecular Medicine · USNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT3 is a latent transcription factor that plays a vital role in the transmission of extracellular signal from receptors to the nucleus. It has been regarded as a master transcription factor due to its role in the regulation of a broad spectrum of genes, which can contribute to oncogenesis. Persistent activation of STAT3 and deregulation of its signaling has been observed in various human cancers including head and neck squamous cell carcinoma (HNSCC). In the present work, we identified brusatol (BT) as a potential blocker of STAT3 signaling pathway in diverse HNSCC cells. The data from the cell-based experiments suggested that BT-induced cytotoxicity and abrogated the activation of STAT3 and that of upstream kinases such as JAK1, JAK2, and Src. It reduced the levels of nuclear STAT3 and its DNA binding ability. BT treatment increased annexin-V-positive cells, promoted procaspase-3 and PARP cleavage, and downregulated the mRNA and protein expression of diverse proteins (Bcl-2, Bcl-xl, survivin) in HNSCC cells. Taken together, brusatol can function as a promising inhibitor targeting STAT3 signaling pathway in HNSCC.

Indexed as

Antineoplastic Agents, PhytogenicCell Line, TumorCell NucleusCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansQuassinsSignal TransductionSquamous Cell Carcinoma of Head and NeckSTAT3 Transcription FactorAntineoplastic Agents, PhytogenicbrusatolQuassinsSTAT3 protein, humanSTAT3 Transcription FactorapoptosisbrusatolHNSCCSTAT3 inhibitor

Identifiers

PMID31575007
PMCPMC6843503
OpenAlexW2976144232

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.