Evidence map›Paper›PMID 37899744›Full record

ArticleBiomolecules & therapeutics2023

Licochalcone H Targets EGFR and AKT to Suppress the Growth of Oxaliplatin -Sensitive and -Resistant Colorectal Cancer Cells.

Seung-On Lee, Mee-Hyun Lee, Ah-Won Kwak, Jin-Young Lee, Goo Yoon, Sang Hoon Joo, Yung Hyun Choi, Jin Woo Park, Jung-Hyun Shim

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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 9 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

9 authors at 6 institutions in 2 countries.

Seung-On LeeDepartment of Biomedicine, Health & Life Convergence Sciences, BK21 Four, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Mee-Hyun LeeCollege of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea.
Ah-Won KwakBiosystem Research Group, Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Republic of Korea.
Jin-Young LeeDepartment of Biological Sciences, Keimyung University, Daegu 42601, Republic of Korea.
Goo YoonDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Sang Hoon JooCollege of Pharmacy, Daegu Catholic University, Gyeongsan 38430, Republic of Korea.
Yung Hyun ChoiDepartment of Biochemistry, College of Korean Medicine, Dong-Eui University, Busan 47227, Republic of Korea.
Jin Woo ParkDepartment of Biomedicine, Health & Life Convergence Sciences, BK21 Four, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Jung-Hyun ShimDepartment of Biomedicine, Health & Life Convergence Sciences, BK21 Four, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea.
Mokpo National University · KRDaegu Catholic University · KRDong-Eui University · KRDongshin University · KRKeimyung University · KRKorea Institute of Toxicology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment of colorectal cancer (CRC) has always been challenged by the development of resistance. We investigated the antiproliferative activity of licochalcone H (LCH), a regioisomer of licochalcone C derived from the root of Glycyrrhiza inflata, in oxaliplatin (Ox)-sensitive and -resistant CRC cells. LCH significantly inhibited cell viability and colony growth in both Ox-sensitive and Ox-resistant CRC cells. We found that LCH decreased epidermal growth factor receptor (EGFR) and AKT kinase activities and related activating signaling proteins including pEGFR and pAKT. A computational docking model indicated that LCH may interact with EGFR, AKT1, and AKT2 at the ATP-binding sites. LCH induced ROS generation and increased the expression of the ER stress markers. LCH treatment of CRC cells induced depolarization of MMP. Multi-caspase activity was induced by LCH treatment and confirmed by Z-VAD-FMK treatment. LCH increased the number of sub-G1 cells and arrested the cell cycle at the G1 phase. Taken together LCH inhibits the growth of Ox-sensitive and Ox-resistant CRC cells by targeting EGFR and AKT, and inducing ROS generation and ER stress-mediated apoptosis. Therefore, LCH could be a potential therapeutic agent for improving not only Ox-sensitive but also Ox-resistant CRC treatment.

Indexed as

AKTApoptosisColorectal cancerEGFRLicochalcone H (LCH)Oxaliplatin

Identifiers

PMID37899744
PMCPMC10616518
OpenAlexW4388013958

What OpenQuestion holds

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LicenceCC BY-NC
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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.