Evidence map›Paper›PMID 34944451›Full record

ArticleBiomolecules2021

Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells.

Kwang-Youn Kim, Un-Jung Yun, Seung-Hee Yeom, Sang-Chan Kim, Hu-Jang Lee, Soon-Cheol Ahn, Kwang-Il Park, Young-Woo Kim

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Hemistepsin A induces apoptosis by modulating the reactive oxygen species-dependent PI3K/Akt signaling pathway in human lung carcinoma A549 cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  2. Review
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

8 authors at 5 institutions in 1 country.

Kwang-Youn KimKorean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu 41062, Korea.ORCID 0000-0003-2471-2611
Un-Jung YunSchool of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
Seung-Hee YeomSchool of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.
Sang-Chan KimMedical Research Center, College of Oriental Medicine, Daegu Haany University, Gyeongsan 38610, Korea.ORCID 0000-0003-0515-0764
Hu-Jang LeeCollege of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea.
Soon-Cheol AhnDepartment of Microbiology & Immunology, Pusan National University School of Medicine, Yangsan 50612, Korea.
Kwang-Il ParkCollege of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea.ORCID 0000-0002-0199-8090
Young-Woo KimSchool of Korean Medicine, Dongguk University, Gyeongju 38066, Korea.ORCID 0000-0002-3323-7106
Daegu Haany University · KRDongguk University · KRGyeongsang National University · KRKorea Institute of Oriental Medicine · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is an essential strategy for cancer treatment. On the other hand, consistent exposure to chemotherapeutic drugs induces chemo-resistance in cancer cells through a variety of mechanisms. Therefore, it is important to develop a new drug inhibiting chemo-resistance. Although hemistepsin A (HsA) is known to have anti-tumor effects, the molecular mechanisms of HsA-mediated cell death are unclear. Accordingly, this study examined whether HsA could induce apoptosis in aggressive prostate cancer cells, along with its underlying mechanism. Using HsA on two prostate cancer cell lines, PC-3 and LNCaP cells, the cell analysis and in vivo xenograft model were assayed. In this study, HsA induced apoptosis and autophagy in PC-3 cells. HsA-mediated ROS production attenuated HsA-induced apoptosis and autophagy after treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger. Moreover, autophagy inhibition by 3-MA or CQ is involved in accelerating the apoptosis induced by HsA. Furthermore, we showed the anti-tumor effects of HsA in mice, as assessed by the reduced growth of the xenografted tumors. In conclusion, HsA induced apoptosis and ROS generation, which were blocked by protective autophagy signaling.

Indexed as

AMP-Activated Protein KinasesAnimalsAutophagyCell Line, TumorCell ProliferationCell SurvivalChloroquineDrug SynergismGene Expression Regulation, NeoplasticHumansLactonesMaleMicePC-3 CellsProstatic NeoplasmsReactive Oxygen SpeciesAMP-Activated Protein KinasesChloroquinehemistepsinLactonesReactive Oxygen SpeciesSesquiterpenesAMPKapoptosisautophagyHemistepsin Aprostate cancerROS

Identifiers

PMID34944451
PMCPMC8699411
OpenAlexW3217681616

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.