Evidence map›Paper›PMID 35053027›Full record

ArticleBiology2021

3-Formylchromone Counteracts STAT3 Signaling Pathway by Elevating SHP-2 Expression in Hepatocellular Carcinoma.

Chakrabhavi Dhananjaya Mohan, Min Hee Yang, Shobith Rangappa, Arunachalam Chinnathambi, Sulaiman Ali Alharbi, Tahani Awad Alahmadi, Amudha Deivasigamani, Kam Man Hui, Gautam Sethi, Kanchugarakoppal S Rangappa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Biology, 2021. 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
2.0field-weighted citation impact, top 10% 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, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Genistein: a promising modulator of apoptosis and survival signaling in cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
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  5. Review
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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

11 authors at 6 institutions in 4 countries.

Chakrabhavi Dhananjaya MohanDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysore 570006, India.
Min Hee YangKHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea.
Shobith RangappaAdichunchanagiri Institute for Molecular Medicine, Adichunchanagiri University, BG Nagara 571448, India.
Arunachalam ChinnathambiDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0001-5075-5901
Sulaiman Ali AlharbiDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Tahani Awad AlahmadiDepartment of Pediatrics, College of Medicine and King Khalid University Hospital, King Saud University, Riyadh 11461, Saudi Arabia.
Amudha DeivasigamaniDivision of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore 169610, Singapore.
Kam Man HuiDivision of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore 169610, Singapore.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore.
Kanchugarakoppal S RangappaInstitution of Excellence, Vijnana Bhavan, University of Mysore, Manasagangotri, Mysore 570006, India.
Kwang Seok AhnKHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea.ORCID 0000-0002-2882-0612
King Saud University · SAKyung Hee University · KRNational Cancer Centre Singapore · SGUniversity of Mysore · INInstitute of Molecular Medicine · INNational University of Singapore · SG

Funding

National Research Foundation of Korea NRF-2021R1I1A2060024
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the leading cancers that contribute to a large number of deaths throughout the globe. The signal transducer and activator of transcription 3 (STAT3) is a tumorigenic protein that is overactivated in several human malignancies including HCC. In the present report, the effect of 3-formylchromone (3FC) on the STAT3 signaling pathway in the HCC model was investigated. 3FC downregulated the constitutive phosphorylation of STAT3 and non-receptor tyrosine kinases such as JAK1 and JAK2. It also suppressed the transportation of STAT3 to the nucleus and reduced its DNA-binding ability. Pervanadate treatment overrode the 3FC-triggered STAT3 inhibition, and the profiling of cellular phosphatase expression revealed an increase in SHP-2 levels upon 3FC treatment. The siRNA-driven deletion of SHP-2 led to reinstate STAT3 activation. 3FC downmodulated the levels of various oncogenic proteins and decreased CXCL12-driven cell migration and invasion. Interestingly, 3FC did not exhibit any substantial toxicity, whereas it significantly regressed tumor growth in an orthotopic HCC mouse model and abrogated lung metastasis. Overall, 3FC can function as a potent agent that can display antitumor activity by targeting STAT3 signaling in HCC models.

Indexed as

apoptosisformylchromonehepatocellular carcinomaSHP-2STAT3 signaling

Identifiers

PMID35053027
PMCPMC8773260
OpenAlexW4200056490

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.