Evidence map›Paper›PMID 26788147›Full record

ArticleOncology letters2015

β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling.

Dan Lu, Jing Qian, Wei Li, Qianqian Feng, Shu Pan, Siquan Zhang

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Review
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  7. Article
  8. Article
  9. Shikonin Mediates Apoptosis through G Protein-Coupled Estrogen Receptor of Ovarian Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. [Shikonin induces cell death by inhibiting glycolysis in human testicular cancer I-10 and seminoma TCAM-2 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  14. Article
  15. Deoxyshikonin isolated fromPharmaceutical biology · 2019
    Article
  16. Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Dan LuDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Jing QianDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Wei LiDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Qianqian FengDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Shu PanDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Siquan ZhangDepartment of Gynecology & Obstetrics, College of Clinical Medicine, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.
Yangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the inhibitory ability of β-hydroxyisovaleryl-shikonin (β-HIVS) on the proliferation of human cervical cancer HeLa cells and to identify the mechanism of this effect. The HeLa cells were treated with β-HIVS and the inhibition of cell growth was detected by an MTT assay. Flow cytometry was performed to analyze the apoptosis rate and cell cycle distribution of HeLa cells. Reverse transcription-polymerase chain reaction and western blot analysis were used to examine the expression of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins. The results revealed that β-HIVS inhibited HeLa cell proliferation in a dose- and time-dependent manner. With the administration of increasing concentrations of β-HIVS, the apoptotic rate of HeLa cells was also increased. The cell cycle was slightly arrested at the S phase, with ~6% of cells in this phase, subsequent to treatment with 10 µM β-HIVS. In addition, β-HIVS markedly reduced the expression levels of PI3K, AKT, mTOR and 70-kDa ribosomal protein S6 kinase in HeLa cells. β-HIVS promoted cervical cancer cell apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression. The present study is expected to lead to the development of molecular targeted therapy for this signaling pathway as a novel method of cervical cancer treatment.

Indexed as

apoptosiscervical cancerHeLa cellsphosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathwayβ-hydroxyisovaleryl shikonin

Identifiers

PMID26788147
PMCPMC4665374
OpenAlexW2145552412

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.