Evidence map›Paper›PMID 41663817›Full record

ArticleApoptosis : an international journal on programmed cell death2026

LncRNA AC098613.1 promotes acute myeloid leukemia cell differentiation through CDC5L/ADAP1/NRD1 axis.

Qingling Jiang, Xiaoting Wang, Hang Yao, Jince Wang, Peiyu Tang, Mingpeng Liang, Zhaohai Pan, Bohan Li, Chunhua Lin, Qinxuan Wu and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Qingling Jiang *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Xiaoting Wang *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Hang Yao *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Jince Wang *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Peiyu TangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Mingpeng LiangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Zhaohai PanFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Bohan LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Chunhua LinDepartment of Urology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264099, Shandong, China.
Qinxuan WuHunan Provincial Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, the "Double-First Class" Application Characteristic Discipline of Hunan Province (Pharmaceutical Science), Changsha Medical University, Changsha, 410219, Hunan, China.
Qi WangHunan Provincial Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, the "Double-First Class" Application Characteristic Discipline of Hunan Province (Pharmaceutical Science), Changsha Medical University, Changsha, 410219, Hunan, China.
Qiusheng ZhengFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China.
Chiu-Fai KuokFaculty of Health Sciences and Sports, Macao Polytechnic University, Macau, 999078, Macao, SAR, China.
Hongfu LiuDepartment of Human Anatomy, College of Basic Medical Sciences, Binzhou Medical University, Yantai, 264003, Shandong, China. liuhongfu95@163.com.
Changgang SunCollege of Traditional Chinese Medicine, Shandong Second Medical University, Weifang, 261053, Shandong, China. scgdoctor@126.com.
Defang LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, 264003, Shandong, China. lidefang@163.com.

Funding

National Natural Science Foundation of China 82073313Natural Science Foundation of Shandong Province ZR2021QH357
6 · The paper itself

Abstract

Recently evidence has suggested that long non-coding RNAs (lncRNAs) play a pivotal role in the prognosis and treatment of leukemia. However, studies on their use in differentiation therapy of acute myeloid leukemia (AML) remain scarce. In this study, we found that AC098613.1 was significantly increased in differentiated THP-1 cells, while its expression was significantly lower in AML patients. Moreover, AC098613.1 overexpression inhibited proliferation and induced differentiation of THP-1 and HL-60 cells. Mechanistically, we found that AC098613.1 targeted cell division cycle 5-like protein (CDC5L) to increase its stability, thereby enhancing its abundance and nuclear localization, and promoted the transcription of ADP-ribosylation factor GTPase activating protein with dual PH domains 1 (ADAP1) and the expression of nardilysin (encoded by NRD1), which ultimately induced the differentiation of AML cells. We further demonstrated in vivo that AC098613.1 overexpression significantly inhibited tumor growth by affecting the stability of CDC5L and regulating the expression of ADAP1, NRD1 and cyclin-dependent kinase 1 (CDK1). The research demonstrates that AC098613.1 promotes AML cell differentiation by regulating the CDC5L/ADAP1/NRD1 axis, providing a new target for AML differentiation therapy.

Indexed as

Adaptor Proteins, Signal TransducingCell Cycle ProteinsCell DifferentiationLeukemia, Myeloid, AcuteRNA, Long NoncodingAnimalsCell Line, TumorCell ProliferationHL-60 CellsHumansMiceTHP-1 CellsAdaptor Proteins, Signal TransducingCell Cycle ProteinsRNA, Long NoncodingAC098613.1Acute myeloid leukemiaDifferentiation

Identifiers

PMID41663817

What OpenQuestion holds

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Registered trials

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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.