Evidence map›Paper›PMID 33627630›Full record

ArticleCell death & disease2021

Suppression of steroid 5α-reductase type I promotes cellular apoptosis and autophagy via PI3K/Akt/mTOR pathway in multiple myeloma.

Renjie Dou, Jinjun Qian, Wei Wu, Yanxin Zhang, Yuxia Yuan, Mengjie Guo, Rongfang Wei, Shu Yang, Artur Jurczyszyn, Siegfried Janz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  7. [Molecular mechanism of high-altitude hypoxia-induced lipid metabolism disorder in mouse spleen tissue].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

13 authors at 4 institutions in 4 countries.

Renjie Dou *The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Jinjun Qian *School of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Wei Wu *The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Yanxin ZhangSchool of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Yuxia YuanSchool of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Mengjie GuoThe Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Rongfang WeiSchool of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Shu YangSchool of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Artur JurczyszynDepartment of Hematology, Jagiellonian University Medical College, Cracow, Poland.ORCID 0000-0001-9796-8365
Siegfried JanzDivision of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, WI, USA.ORCID 0000-0002-2229-5511
Meral BeksacDepartment of Hematology, School of Medicine, Ankara University, Ankara, Turkey.
Chunyan GuThe Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China. guchunyan@njucm.edu.cn.ORCID 0000-0001-7408-8840
Ye YangThe Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China. yangye876@sina.com.
Nanjing University of Chinese Medicine · CNAnkara University · TRJagiellonian University · PLMedical College of Wisconsin · US

Funding

Defining genetic pathways of plasma-cell neoplasiaR01CA151354 · NCI · UNIVERSITY OF IOWA · PI JANZ, SIEGFRIED · 2010 to 2022
$3.9M
NCI NIH HHS R01 CA151354
6 · The paper itself

Abstract

Steroid 5α-reductase type I (SRD5A1) is a validated oncogene in many sex hormone-related cancers, but its role in multiple myeloma (MM) remains unknown. Based on gene expression profiling (GEP) of sequential MM samples during the disease course, we found that the aberrant expression of SRD5A1 was correlated with progression and poor prognosis in MM patients. In this study, the oncogenic roles of SRD5A1 were validated in human MM cell lines (ARP1 and H929) and the xenograft MM model as well as the 5TMM mouse model. MTT and flow cytometry were used to assess MM cell proliferation, cell cycle, and apoptosis post inducible knockdown SRD5A1 by lentivirus-mediated short-hairpin RNA (shRNA). Transcriptomic sequencing, immunofluorescence, and western blot were used to investigate the effects of SRD5A1 suppression on cell apoptosis and autophagy. Mechanistically, SRD5A1 downregulation simultaneously regulated both the Bcl-2 family protein-mediated apoptosis and the autophagic process via PI3K/Akt/mTOR signaling pathway in MM cells. Meanwhile, the autophagy inhibitor (3-methyladenine) and SRD5A1 inhibitor (Dutasteride) were utilized to evaluate their anti-myeloma effect. Thus, our results demonstrated that SRD5A1 downregulation simultaneously regulated both the apoptosis and the autophagic process in MM cells. The dual autophagy-apoptosis regulatory SRD5A1 may serve as a biomarker and potential target for MM progression and prognosis.

Indexed as

ApoptosisAutophagy3-Oxo-5-alpha-Steroid 4-Dehydrogenase5-alpha Reductase InhibitorsAdenineAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationDutasterideEnzyme RepressionFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane Proteins3-methyladenine3-Oxo-5-alpha-Steroid 4-Dehydrogenase5-alpha Reductase InhibitorsAdenineAntineoplastic AgentsDutasterideMembrane ProteinsMTOR protein, humanmTOR protein, mousePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSRD5A1 protein, humanSrd5a1 protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID33627630
PMCPMC7904855
OpenAlexW3130285568

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.