Evidence map›Paper›PMID 37764501›Full record

ArticleMolecules (Basel, Switzerland)2023

Shikonin Causes an Apoptotic Effect on Human Kidney Cancer Cells through Ras/MAPK and PI3K/AKT Pathways.

József Király, Erzsébet Szabó, Petra Fodor, Zsolt Fejes, Béla Nagy, Éva Juhász, Anna Vass, Mahua Choudhury, Gábor Kónya, Gábor Halmos and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. 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
4.9field-weighted citation impact, top 4% 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, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. 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

11 authors at 2 institutions in 2 countries.

József KirályDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Erzsébet SzabóDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Petra FodorDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Zsolt FejesDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0002-1387-2970
Béla NagyDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0002-5700-3267
Éva JuhászDepartment of Pediatrics, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Anna VassDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Mahua ChoudhuryDepartment of Pharmaceutical Sciences, Irma Lerma Rangel School of Pharmacy, Texas A&M Health Science Center, College Station, TX 77845, USA.
Gábor KónyaDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Gábor HalmosDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
Zsuzsanna SzabóDepartment of Biopharmacy, Faculty of Pharmacy, University of Debrecen, 4032 Debrecen, Hungary.
University of Debrecen · HUTexas A&M Health Science Center · US

Funding

European Union and the European Regional Development Fund GINOP-2.3.4-15-2016-00002Thematic Excellence Program TKP2021-EGA-19
6 · The paper itself

Abstract

(1) Background: Shikonin, the main ingredient in Chinese herbal medicine, is described as a novel angiogenesis inhibitor, and its anticancer effects have already been studied. Shikonin and its derivatives induce apoptosis and suppress metastasis, which further enhance the effectiveness of chemotherapy. However, their mechanism of function has not been completely elucidated on human renal cancer cells. (2) Methods: In our study, CAKI-2 and A-498 cells were treated with increasing concentrations (2.5-40 µM) of shikonin, when colony formation ability and cytotoxic activity were tested. The changes in the expression of the main targets of apoptotic pathways were measured by RT-qPCR and Western blot. The intracellular levels of miR-21 and miR-155 were quantified by RT-qPCR. (3) Results: Shikonin exerted a dose-dependent effect on the proliferation of the cell lines examined. In 5 µM concentration of shikonin in vitro elevated caspase-3 and -7 levels, the proteins of the Ras/MAPK and PI3K/AKT pathways were activated. However, no significant changes were detected in the miR-21 and miR-155 expressions. (4) Conclusions: Our findings indicated that shikonin causes apoptosis of renal cancer cells by activating the Ras/MAPK and PI3K/AKT pathways. These effects of shikonin on renal cancer cells may bear important potential therapeutic implications for the treatment of renal cancer.

Indexed as

ApoptosisKidney NeoplasmsNaphthoquinonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMicroRNAsras ProteinsMicroRNAsMIRN155 microRNA, humanMIRN21 microRNA, humanNaphthoquinonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktras ProteinsshikoninA-498apoptosisCAKI-2human renal cancerRas/MAPK and PI3K/AKT pathwaysshikonintargeted therapy

Identifiers

PMID37764501
PMCPMC10534756
OpenAlexW4386879710

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.