Related Experiment Video

Updated: Oct 16, 2025

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

336

CDC45 modulates MCM7 expression and inhibits cell proliferation by suppressing the PI3K/AKT pathway in acute myeloid

Rong Zhang1, Zhuogang Liu1, Guojun Zhang1

  • 1Department of Hematology, Shenjing Hospital of China Medical University Shenyang, Liaoning Province, People's Republic of China.

American Journal of Translational Research
|October 15, 2021
PubMed

Insights

This study identifies CDC45 and MCM7 as potential diagnostic and therapeutic targets for acute myeloid leukemia (AML). Their expression levels correlate with treatment outcomes and disease progression, suggesting a role in AML pathogenesis.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Acute myeloid leukemia (AML) is a complex hematologic malignancy with a generally poor prognosis.
  • Identifying novel diagnostic and therapeutic targets is crucial for improving AML patient outcomes.

Purpose of the Study:

  • To identify novel molecular targets for the diagnosis and treatment of acute myeloid leukemia (AML).
  • To investigate the functional roles and interrelationships of potential key genes in AML pathogenesis.

Main Methods:

  • Differential gene expression analysis of AML patient data from Gene Expression Omnibus (GEO) datasets (GSE65409, GSE90062) using GEO2R.
  • Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of differentially expressed genes (DEGs) via DAVID.
  • Protein-protein interaction network analysis using STRING to identify hub genes (CDC45, MCM7).
  • Validation of gene expression using GEO and The Cancer Genome Atlas (TCGA) databases.
  • Correlation analysis, gene overexpression studies, cell proliferation assays, and cell cycle analysis.
  • Investigation of the PI3K/AKT/mTOR signaling pathway.

Main Results:

  • Two potential hub genes, CDC45 and MCM7, were identified as differentially expressed in AML.
  • Both CDC45 and MCM7 were found to be downregulated in AML specimens compared to normal controls.
  • High expression of CDC45 correlated positively with complete remission and negatively with key clinical parameters.
  • High expression of MCM7 correlated negatively with clinical parameters and unfavorable cytogenetics.
  • Overexpression of CDC45 or MCM7 impaired AML cell proliferation and induced G1/S phase arrest.
  • Overexpression of either gene attenuated PI3K/AKT/mTOR signaling; MCM7 knockdown reversed CDC45 overexpression effects.

Conclusions:

  • CDC45 and MCM7 are significantly downregulated in AML and exhibit a functional relationship.
  • These genes may serve as potential biomarkers for AML diagnosis and prognosis.
  • Targeting CDC45 and MCM7, possibly through the PI3K/AKT/mTOR pathway, could offer new therapeutic strategies for AML.
Keywords:
Acute myeloid leukemiaCDC45MCM7cell cyclecell proliferation

More Related Videos

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

10.1K
Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation09:09

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

Published on: November 10, 2017

8.5K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.7K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.9K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.8K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.2K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.0K