Evidence map›Paper›PMID 37740843›Full record

ArticleJournal of molecular histology2023

Sennoside A induces autophagic death of prostate cancer via inactivation of PI3K/AKT/mTOR axis.

Shaoyi Qiao, Wuhe Zhang, Yao Jiang, Yansheng Su

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Silencing APLNR enhances the radiosensitivity of prostate cancer by modulating the PI3K/AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  9. 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

4 authors at 2 institutions in 1 country.

Shaoyi QiaoDepartment of Urology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an, Shaanxi, 710054, China.
Wuhe ZhangDepartment of Urology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an, Shaanxi, 710054, China. Zhangwuheuro@21cn.com.ORCID http://orcid.org/0000-0001-5339-366X
Yao JiangDepartment of Urology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an, Shaanxi, 710054, China.
Yansheng SuDepartment of Urology, Xijing 986 Hospital Department, Fourth Military Medical University, Xi'an, Shaanxi, 710054, China.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PC) is the most common malignancy in male reproductive system. Sennoside A (SA) is an anthraquinone active ingredient extracted from Rheum officinale Baill., which exerts anti-tumor activity on different tumors. In the present study, the toxicity of SA on PC3 and DU 145 cells was detected via CCK-8. The effects of SA on growth, apoptosis, and autophagy were determined through CCK-8, Hoechst stain, flow cytometry, western blot, and immunofluorescence examinations. An in vivo experiment was performed in xenografted mice with intraperitoneal introduction of 10 mg/kg SA and validated via TUNEL, immunohistochemistry and western blot. The results showed that SA inhibited the cell viability with a IC50 value of 52.36 and 67.48 µM in DU 145 and PC3 cells respectively, and enhanced the apoptosis of PC3 and DU 145 cells. Additionally, SA elevated the relative LC3B expression, and the relative protein expression of LC3II/LC3I and Beclin-1, but diminished the P62 protein expression. The relative protein level of p-PI3K/PI3K, p-AKT/AKT and p-mTOR/mTOR was reduced with SA treatment, which was verified by the 740 Y-P application. The 740 Y-P treatments also restored the SA-induced the cell viability, apoptosis rate and relative LC3B expression. Meanwhile, SA inhibited the growth of PC cell and the relative protein level of PI3K/AKT/mTOR axis in vivo. Taken together, SA regulated the proliferation, apoptosis and autophagy via inactivating the PI3K/AKT/mTOR axis in PC.

Indexed as

Prostatic NeoplasmsProto-Oncogene Proteins c-aktAnimalsApoptosisAutophagyCell Line, TumorCell ProliferationHumansMaleMicePhosphatidylinositol 3-KinasesSennosidesSignal TransductionSincalideTOR Serine-Threonine KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSennosidesSincalideTOR Serine-Threonine KinasesApoptosisAutophagyPI3K/AKT/mTORProliferationProstate cancerSennoside A

Identifiers

PMID37740843
OpenAlexW4386988234

What OpenQuestion 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 OpenQuestion graph.