Evidence map›Paper›PMID 39898241›Full record

ArticleInternational journal of medical sciences2025

NACC1 accelerates the progression of AML by regulating the ADAM9/PI3K/AKT axis.

Ying Zhang, Liang Zhong, Peng Wan, Yi Zhao, Meng Wang, Hongyan Zhang, Yang Liao, Ying Deng, Beizhong Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of medical sciences, 2025. 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
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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.

  1. Review
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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

9 authors.

Ying ZhangCentral Laboratory of Yongchuan 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.
Peng WanCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Yi ZhaoCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Meng WangCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Hongyan ZhangCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Yang LiaoCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Ying DengCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
Beizhong LiuCentral Laboratory of Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nucleus accumbens-associated protein 1 (NACC1) regulates various types of biological processes. It is a transcription factor associated with cancer. NACC1 is overexpressed in many human malignancies and can regulate the progression, metastasis, and drug resistance of cancer cells. However, its precise role in acute myeloid leukemia (AML) remains unknown. This study aimed to unravel the basic mechanism of NACC1 in AML. Our findings demonstrated that NACC1 is immensely expressed in AML cells. Lentiviral vector-mediated knockdown of NACC1 inhibited the PI3K/AKT signaling pathway. Simultaneously, NACC1 knockdown promoted apoptosis, suppressed the proliferative capacity of AML cells, and resulted in cell cycle arrest during the G0/G1 phase. Additionally, A disintegrin and metalloproteinase 9 (ADAM9) was markedly expressed in AML cells. NACC1 regulated ADAM9 expression. ADAM9 expression was also downregulated after NACC1 knockdown. Concurrently, ADAM9 knockdown affected the activity of AML cells by decelerating the growth rate, promoting apoptosis, and blocking cell cycle progression. In addition, the AKT activator SC79 restored the inhibited cell proliferation after NACC1 knockdown and ADAM9 knockdown. In conclusion, our study suggested that the NACC1/ADAM9/PI3K/AKT axis is crucial for sustaining the survival of AML cells, indicating that NACC1 may be a viable target for treating AML.

Indexed as

ADAM ProteinsLeukemia, Myeloid, AcuteMembrane ProteinsApoptosisCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionADAM9 protein, humanADAM ProteinsMembrane ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAcute myeloid leukemiaADAM9Cell apoptosisNACC1PI3K/AKT pathwayProliferation

Identifiers

PMID39898241
PMCPMC11783076

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