Evidence map›Paper›PMID 37899745›Full record

ArticleBiomolecules & therapeutics2023

Licochalcone D Inhibits Skin Epidermal Cells Transformation through the Regulation of AKT Signaling Pathways.

Sun-Young Hwang, Kwanhwan Wi, Goo Yoon, Cheol-Jung Lee, Soong-In Lee, Jong-Gil Jung, Hyun-Woo Jeong, Jeong-Sang Kim, Chan-Heon Choi, Chang-Su Na and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Biomolecules & therapeutics, 2023. 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
2.5field-weighted citation impact, top 12% 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, 10 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

12 authors at 3 institutions in 1 country.

Sun-Young HwangCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Kwanhwan WiCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Goo YoonDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Cheol-Jung LeeResearch Center for Materials Analysis, Korea Basic Science Institute, Daejeon 34133, Republic of Korea.
Soong-In LeeCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Jong-Gil JungCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Hyun-Woo JeongCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Jeong-Sang KimCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Chan-Heon ChoiCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Chang-Su NaCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Jung-Hyun ShimDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Mee-Hyun LeeCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Dongshin University · KRMokpo National University · KRKorea Basic Science Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell transformation induced by epidermal growth factor (EGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA) is a critical event in cancer initiation and progression, and understanding the underlying mechanisms is essential for the development of new therapeutic strategies. Licorice extract contains various bioactive compounds, which have been reported to have anticancer and anti-inflammatory effects. This study investigated the cancer preventive efficacy of licochalcone D (LicoD), a chalcone derivative in licorice extract, in EGF and TPA-induced transformed skin keratinocyte cells. LicoD effectively suppressed EGF-induced cell proliferation and anchorage-independent colony growth. EGF and TPA promoted the S phase of cell cycle, while LicoD treatment caused G1 phase arrest and down-regulated cyclin D1 and up-regulated p21 expression associated with the G1 phase. LicoD also induced apoptosis and increased apoptosis-related proteins such as cleaved-caspase-3, cleaved-caspase-7, and Bax (Bcl-2-associated X protein). We further investigated the effect of LicoD on the AKT signaling pathway involved in various cellular processes and found decreased p-AKT, p-GSK3β, and p-NFκB expression. Treatment with MK-2206, an AKT pharmacological inhibitor, suppressed EGF-induced cell proliferation and transformed colony growth. In conclusion, this study demonstrated the potential of LicoD as a preventive agent for skin carcinogenesis.

Indexed as

AKT SignalingCell TransformationEGFLicochalcone D (LicoD)TPA

Identifiers

PMID37899745
PMCPMC10616519
OpenAlexW4388014090

What OpenQuestion holds

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LicenceCC BY-NC
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.