Evidence map›Paper›PMID 34873073›Full record

ArticleBiomolecules & therapeutics2022

Licochalcone H Induces Cell Cycle Arrest and Apoptosis in Human Skin Cancer Cells by Modulating JAK2/STAT3 Signaling.

Kyung-Ho Park, Sang Hoon Joo, Ji-Hye Seo, Jumi Kim, Goo Yoon, Young-Joo Jeon, Mee-Hyun Lee, Jung-Il Chae, Woo-Keun Kim, Jung-Hyun Shim

Open access · hybridAbstract read
In one paragraph

Article in Biomolecules & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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  9. AnIranian journal of basic medical sciences · 2023
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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

10 authors at 6 institutions in 2 countries.

Kyung-Ho ParkDepartment of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Sang Hoon JooCollege of Pharmacy, Daegu Catholic University, Gyeongsan 38430, Republic of Korea.
Ji-Hye SeoDepartment of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Jumi KimDepartment of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Goo YoonDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Young-Joo JeonStem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea.
Mee-Hyun LeeCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Jung-Il ChaeDepartment of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Woo-Keun KimBiosystem Research Group, Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Republic of Korea.
Jung-Hyun ShimDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Jeonbuk National University · KRMokpo National University · KRCatholic University of Daegu · KRDongshin University · KRKorea Institute of Toxicology · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Licochalcone H (LCH) is a phenolic compound synthetically derived from licochalcone C (LCC) that exerts anticancer activity. In this study, we investigated the anticancer activity of LCH in human skin cancer A375 and A431 cells. The 3-(4,5-dimethylthiazol- 2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) cell viability assay was used to evaluate the antiproliferative activity of LCH. Cell cycle distribution and the induction of apoptosis were analyzed by flow cytometry. Western blotting assays were performed to detect the levels of proteins involved in cell cycle progression, apoptosis, and the JAK2/STAT3 signaling pathway. LCH inhibited the growth of cells in dose- and time-dependent manners. The annexin V/propidium iodide double staining assay revealed that LCH induced apoptosis, and the LCH-induced apoptosis was accompanied by cell cycle arrest in the G1 phase. Western blot analysis showed that the phosphorylation of JAK2 and STAT3 was decreased by treatment with LCH. The inhibition of the JAK2/STAT3 signaling pathway by pharmacological inhibitors against JAK2/STAT3 (cryptotanshinone (CTS) and S3I-201) simulated the antiproliferative effect of LCH suggesting that LCH induced apoptosis by modulating JAK2/STAT3 signaling.

Indexed as

ApoptosisHuman skin cancerJAK2Licochalcone HSTAT3

Identifiers

PMID34873073
PMCPMC8724845
OpenAlexW4200135503

What OpenQuestion holds

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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.