Evidence map›Paper›PMID 35370472›Full record

ArticleInternational journal of medical sciences2022

RIP1-dependent Apoptosis and Differentiation Regulated by Skp2 and Akt/GSK3β in Acute Myeloid Leukemia.

Wenran Dan, Liang Zhong, Zhonghui Zhang, Peng Wan, Yang Lu, Xiao Wang, Zhenyan Liu, Xuan Chu, Beizhong Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of medical sciences, 2022. 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
0.4field-weighted citation impact, top 42% 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, 5 citations in OpenAlex.

  1. Article
  2. The roles of ubiquitination in AML.Annals of hematology · 2024
    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

9 authors at 1 institution in 1 country.

Wenran DanCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Liang ZhongKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.
Zhonghui ZhangCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Peng WanCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Yang LuCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Xiao WangCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Zhenyan LiuCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Xuan ChuCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Beizhong LiuCentral Laboratory of Yong-Chuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a heterogeneous neoplasm characterized by variations in cytogenetics and molecular abnormalities, which result in variable response to therapy. Receptor-interacting serine/threonine kinase 1 (RIP1)-mediated necroptosis has been reported to have a potential role in the treatment of AML. We obtained Skp2 and RIP1 are significantly overexpressed in AML samples using original published data, and identified that Skp2-depletion in AML cells significantly suppressed RIP1. Functional analysis showed that the inhibition of RIP1 caused by necrostatin-1 (Nec-1) inhibited the proliferation, simultaneously facilitate both the apoptosis and differentiation of AML cells. Mechanistical analysis elucidated that knockdown of Skp2 suppresses RIP1 by transcriptional regulation but not by proteasome degradation. Additionally, Skp2 regulated the function of RIP1 by decreasing K63-linked ubiquitin interaction with RIP1. Moreover, the suppression of Akt/GSK3β was observed in Skp2 knockdown stable NB4 cells. Also, GSK3β inactivation via small-molecule inhibitor treatment remarkably decreased RIP1 level. RIP1 regulates differentiation by interacting with RARα, increasing RA signaling targets gene C/EBPα and C/EBPβ. In conclusion, our study provides a novel insight into the mechanism of tumorigenesis and the development of AML, for which the Skp2-Akt/GSK3β-RIP1 pathway can be developed as a promising therapeutic target.

Indexed as

Leukemia, Myeloid, AcuteProto-Oncogene Proteins c-aktApoptosisCell DifferentiationGlycogen Synthase Kinase 3 betaHumansS-Phase Kinase-Associated ProteinsGlycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene Proteins c-aktSKP2 protein, humanS-Phase Kinase-Associated ProteinsAcute myelocytic leukemiaGSK3βRIP1Skp2

Identifiers

PMID35370472
PMCPMC8964317
OpenAlexW4225558422

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.