Evidence map›Paper›PMID 33982329›Full record

ArticleJournal of gastroenterology and hepatology2021

A curcumin analog GL63 inhibits the malignant behaviors of hepatocellular carcinoma by inactivating the JAK2/STAT3 signaling pathway via the circular RNA zinc finger protein 83/microRNA-324-5p/cyclin-dependent kinase 16 axis.

Ji-An Zhao, Wenjia Nie, Liang Dong, Wencong Liu, Wei Wei

Open access · hybridAbstract read
In one paragraph

Article in Journal of gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. The role of curcumin in modulating circular RNAs and long non-coding RNAs in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  3. Review
  4. Review
  5. Circular RNAs in Cell Cycle Regulation of Cancers.International journal of molecular sciences · 2024
    Review
  6. Article
  7. 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

5 authors at 1 institution in 1 country.

Ji-An ZhaoDepartment of General Surgery, The First Hospital, Hebei Medical University, Shijiazhuang, China.
Wenjia NieDepartment of Medical Service, The First Hospital, Hebei Medical University, Shijiazhuang, China.
Liang DongDepartment of Medical Service, The First Hospital, Hebei Medical University, Shijiazhuang, China.
Wencong LiuDepartment of Ultrasonography, The First Hospital, Hebei Medical University, Shijiazhuang, China.
Wei WeiDepartment of Burn and Plastic Surgery, The First Hospital, Hebei Medical University, Shijiazhuang, China.ORCID https://orcid.org/0000-0001-7297-6190
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aim(1E,4E)-1,5-bis(2-bromophenyl) penta-1,4-dien-3-one (GL63) is a curcumin analog that can protect against carcinogenesis in hepatocellular carcinoma (HCC). The aim of this study was to explore the molecular mechanism of GL63 in HCC.

methodsCell viability was examined by cell counting kit-8 (CCK-8) assay. Circular RNA zinc finger protein 83 (circZNF83), microRNA-324-5p (miR-324-5p), and cyclin-dependent kinase 16 (CDK16) levels were measured via the quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using colony formation assay. Flow cytometry was performed for detecting cell cycle and apoptosis. Protein analysis was conducted by western blot. Cell migration and invasion were determined using transwell assay. Target relation was analyzed using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The function of GL63 in vivo was researched by xenograft model in mice.

resultsGL63 inhibited the circZNF83 expression in HCC cells. CircZNF83 overexpression attenuated the inhibitory effects of GL63 on HCC cell growth, cell cycle progression, migration, and invasion but the promoting effect on cell apoptosis. CircZNF83 served as a sponge of miR-324-5p and circZNF83/miR-324-5p axis was involved in the functional regulation of GL63 in HCC progression. Moreover, CDK16 was a downstream target of miR-324-5p and circZNF83 could regulate the CDK16 expression by sponging miR-324-5p. The anti-tumor function of GL63 was also related to the miR-324-5p/CDK16 axis. In addition, GL63 inactivated the JAK2/STAT3 pathway via downregulating circZNF83 to mediate the miR-324-5p/CDK16 axis. GL63 also repressed tumor growth in vivo through the circZNF83/miR-324-5p/CDK16-mediated JAK2/STAT3 signal inhibition.

conclusionThis study suggested GL63 impeded the HCC development by blocking the JAK2/STAT3 signaling pathway via mediating the circZNF83/miR-324-5p/CDK16 axis.

Indexed as

Carcinoma, HepatocellularCurcuminLiver NeoplasmsMicroRNAsAnimalsCell Line, TumorCyclin-Dependent KinasesMiceRNA, CircularSignal TransductionZinc FingersCurcuminCyclin-Dependent KinasesMicroRNAsRNA, CircularCDK16circZNF83GL63hepatocellular carcinomaJAK2/STAT3 pathwaymiR-324-5p

Identifiers

PMID33982329
PMCPMC8518784
OpenAlexW3160942757

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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.