Evidence map›Paper›PMID 39051078›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024

[Calenduloside E inhibits hepatocellular carcinoma cell proliferation and migration by down-regulating GPX4 and SLC7A11 expression through the autophagy pathway].

Q Chen, S Shang, H Lu, S Li, Z Sun, X Fan, Z Qi

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Q ChenDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
S ShangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
H LuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
S LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
Z SunDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
X FanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.
Z QiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wannan Medical College, Wuhu 241002, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the molecular mechanism through which calenduloside E inhibits hepatocellular carcinoma (HCC) cell proliferation and migration.

methodsHCC cell lines HepG2 and Huh7 treated with calenduloside E were examined for changes in cell viability using CCK-8 assay and expressions of GPX4, SLC7A11, LC3, P62 and phosphorylation of Akt/mTOR using Western blotting. The effects LY294002 and Rapamycin (the inhibitor and activator of autophagy, respectively) on proliferation and migration of calenduloside E-treated HCC cells were evaluated using EdU and Transwell assays. The TCGA database was used to explore the expression levels of GPX4 and SLC7A11 in HCC and normal liver tissues and their correlation with the patients'survival outcomes. GPX4 and SLC7A11 expressions were also detected in HCC cells and normal hepatocytes using RT-qPCR and Western blotting.

resultsCalenduloside E obviously inhibited the viability of HCC cells. GPX4 and SLC7A11 were highly expressed in HCC tissues and cell lines, and their expression levels were negatively correlated with the patients'survival. In HCC cell lines, calenduloside E significantly inhibited the expressions of GPX4 and SLC7A11 proteins, activated the Akt-mTOR pathway, and enhanced the expression of LC3 Ⅱ. The inhibitory effect of calenduloside E on GPX4 and SLC7A11 expressions was significantly enhanced by rapamycin but attenuated by LY294002. Inhibiting the autophagy pathway obviously diminished the inhibitory effect of calenduloside E on proliferation and migration of HCC cells, while activating this pathway produced the opposite effect.

conclusionCalenduside E inhibits the proliferation and migration of HCC cells by down-regulating GPX4 and SLC7A11 expression via the autophagy pathway.

Indexed as

Amino Acid Transport System y+AutophagyCarcinoma, HepatocellularCell MovementCell ProliferationLiver NeoplasmsPhospholipid Hydroperoxide Glutathione PeroxidaseCell Line, TumorDown-RegulationHep G2 CellsHumansOleanolic AcidSaponinsSignal TransductionAmino Acid Transport System y+calenduloside EOleanolic AcidPhospholipid Hydroperoxide Glutathione PeroxidaseSaponinsSLC7A11 protein, humanautophagycalenduside Eglutathione peroxidase 4hepatocellular carcinomasolute carrier family 7 member 11

Identifiers

PMID39051078
PMCPMC11270671

What Socratic holds

Textmetadata
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 Socratic graph.