Evidence map›Paper›PMID 31688993›Full record

ArticleThe Kaohsiung journal of medical sciences2020

Paris saponin VII enhanced the sensitivity of HepG2/ADR cells to ADR via modulation of PI3K/AKT/MAPK signaling pathway.

Gong-En Tang, Yue-Xiang Niu, Yun Li, Chao-Yu Wu, Xiao-Ying Wang, Jian Zhang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. The role ofHeliyon · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Gong-En TangDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.ORCID https://orcid.org/0000-0002-5448-857X
Yue-Xiang NiuDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.
Yun LiDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.
Chao-Yu WuDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.
Xiao-Ying WangDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.
Jian ZhangDepartment of Infectious Disease, Linyi Central Hospital, Linyi, China.
Linyi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To find the effect of Paris saponin VII (PS VII)-mediated PI3K/AKT/MAPK signaling pathway on the sensitivity of ADR-resistant HepG2 cell (HepG2/ADR) cells to ADR. The proliferation inhibitory rates were detected by using MTT assay. Flow cytometry was employed to examine the intracellular accumulation of ADR. The expressions of drug-resistant genes (P-gp, MRP and BCRP) were detected by qRT-PCR, cell apoptosis by Annexin-V-FITC/PI staining, and the expressions of drug-resistance-related proteins, apoptosis-related proteins, and PI3K/AKT/MAPK pathway-related proteins were determined by Western blotting. HepG2/ADR and HepG2 cells treated with PS VII (0.88, 1.32, 1.98, and 2.97 μM) for 48 hours showed increased proliferation inhibitory rate in a dose-dependent manner. HepG2/ADR cells treated PS VII (0.88, 1.32, 1.98 μM) for 48 hours showed decreased IC50 of ADR. Compared with HepG2/ADR cells treated with ADR (5 nM), those treated with PS VII (≤1.98 μM) and ADR (5 nM) showed enhanced ADR accumulation, decreased drug-resistant gene expressions, increased cell apoptosis with unregulated Bax and cleaved caspase-3 and downregulated Bcl-2, as well as the inhibition of PI3K/AKT/MAPK pathway. Moreover, the combination of ADR (5 nM), PS VII (1.98 μM), and LY294002 (PI3K/AKT inhibitor, 20 μM)/SB203580 (P38 inhibitor, 20 μM) for 48 hours could further decreased the HepG2/ADR cell viability, but induced cell apoptosis, accompanying with the decreased expressions of drug-resistant genes. PS VII could downregulate the expressions of drug-resistance genes, increase intracellular accumulation of ADR, promote cell apoptosis, and enhance the sensitivity of HepG2/ADR cells to ADR via PI3K/AKT/MAPK.

Indexed as

ApoptosisDoxorubicinDrug Resistance, NeoplasmHep G2 CellsHumansMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSaponinsSignal TransductionDoxorubicinMitogen-Activated Protein Kinase KinasesParis saponin VIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSaponinsADRhepatocellular carcinomaHepG2Paris saponin VIIPI3K/AKT/MAPK

Identifiers

PMID31688993
PMCPMC11896176
OpenAlexW2982898777

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.