Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells

Wang, Jiazhen; Wang, Peipei; Zhang, Tiantian; Gao, Zhuying; Wang, Jing; Feng, Mengdie; Yin, Rong; Zhang, Haojian

doi:10.1097/bs9.0000000000000020

Cited by 9 publications

(8 citation statements)

References 99 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tumor stem cells can remain dormant for a long period of time and are insensitive to a variety of unfavorable risk factors, which play critical roles in tumor initiation, progression, recurrence, and metastasis [ 116 , 117 ]. It has been shown that tumor stem cells exhibit enhancement for ER stress resistance, which contributes to tumor growth, angiogenesis, and resistance to chemotherapy [ 118 , 119 ].…”

Section: Ncrnas Regulate Upr In Cancer Progressionmentioning

confidence: 99%

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Zhao

Zeng

2020

J Hematol Oncol

View full text Add to dashboard Cite

To survive, cancer cells are subjected to various internal and external adverse factors, including genetic mutations, hypoxia, nutritional deficiencies, and drug toxicity. All of these factors result in the accumulation of unfolded proteins in the endoplasmic reticulum, which leads to a condition termed endoplasmic reticulum stress (ER stress) and triggers the unfolded protein response (UPR). UPR downstream components strictly control transcription and translation reprogramming to ensure selective gene expression, including that of non-coding RNA (ncRNAs), to adapt to adverse environments. NcRNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play important roles in regulating target gene expression and protein translation, and their aberrant expression is related to tumor development. Dysregulation of ncRNAs is involved in the regulation of various cellular characteristics of cancer cells, including growth, apoptosis, metastasis, angiogenesis, drug sensitivity, and tumor stem cell properties. Notably, ncRNAs and ER stress can regulate each other and collaborate to determine the fate of tumor cells. Therefore, investigating the interaction between ER stress and ncRNAs is crucial for developing effective cancer treatment and prevention strategies. In this review, we summarize the ER stress-triggered UPR signaling pathways involved in carcinogenesis followed by the mutual regulation of ER stress and ncRNAs in cancer, which provide further insights into the understanding of tumorigenesis and therapeutic strategies.

show abstract

Section: Ncrnas Regulate Upr In Cancer Progressionmentioning

confidence: 99%

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Zhao

Zeng

2020

J Hematol Oncol

View full text Add to dashboard Cite

show abstract

“…Stemness of leukaemic cells is a major contributor to AML leukaemogenesis and LSCs play a significant role in disease relapse [16].…”

Section: Mirnas and Stemnessmentioning

confidence: 99%

“…Stemness of leukaemic cells is a major contributor to AML leukaemogenesis and LSCs play a significant role in disease relapse [ 16 ]. Recent studies have highlighted the role of mir‐125 in leukaemogenesis and haematopoietic stem cell (HSC) self‐renewal in Mixed Lineage Leukaemia (MLL)‐translocated AML, whereby miR‐125a overexpression upregulated vascular endothelial growth factor A (VEGFA) and was associated with a significantly reduced median survival in MLL/miR‐125 transduced mice.…”

Section: Introductionmentioning

confidence: 99%

microRNA expression in acute myeloid leukaemia: New targets for therapy?

Fletcher

Brown

Javadala

et al. 2022

eJHaem

View full text Add to dashboard Cite

Recent studies have shown that short non-coding RNAs, known as microRNAs (miR-NAs) and their dysregulation, are implicated in the pathogenesis of acute myeloid leukaemia (AML). This is due to their role in the control of gene expression in a variety of molecular pathways. Therapies involving miRNA suppression and replacement have been developed. The normalisation of expression and the subsequent impact on AML cells have been investigated for some miRNAs, demonstrating their potential to act as therapeutic targets. Focussing on miRs with therapeutic potential, we have reviewed those that have a significant impact on the aberrant biological processes associated with AML, and crucially, impact leukaemic stem cell survival. We describe six miRNAs in preclinical trials (miR-21, miR-29b, miR-126, miR-181a, miR-223 and miR-196b) and two miRNAs that are in clinical trials (miR-29 and miR-155). However none have been used to treat AML patients and greater efforts are needed to develop miRNA therapies that could benefit AML patients in the future.

show abstract

“…As a highly heterogeneous disease, both intrinsic and microenvironmental abnormalities participate in the transformation, progression and relapse of AML [ 2 – 4 ]. Elucidating the mechanisms causing adverse phenotypes of AML including exuberant proliferation [ 5 ], more leukemia stem cells (LSCs) [ 6 , 7 ], massive extramedullary dissemination [ 2 ], etc. will provide clues for better outcome.…”

Section: Introductionmentioning

confidence: 99%

Sox13 and M2-like leukemia-associated macrophages contribute to endogenous IL-34 caused accelerated progression of acute myeloid leukemia

Zhang

Cui

et al. 2023

Cell Death Dis

View full text Add to dashboard Cite

Interleukin 34 (IL-34) mainly plays physiologic and pathologic roles through the sophisticated multi-ligand signaling system, macrophage colony-stimulating factor (M-CSF, CSF-1)/IL-34-CSF-1R axis, which exhibits functional redundancy, tissue-restriction and diversity. This axis is vital for the survival, differentiation and function of monocytic lineage cells and plays pathologic roles in a broad range of diseases. However, the role of IL-34 in leukemia has not been established. Here MLL-AF9 induced mouse acute myeloid leukemia (AML) model overexpressing IL-34 (MA9-IL-34) was used to explore its role in AML. MA9-IL-34 mice exhibited accelerated disease progression and short survival time with significant subcutaneous infiltration of AML cells. MA9-IL-34 cells showed increased proliferation. In vitro colony forming assays and limiting dilution transplantation experiments demonstrated that MA9-IL-34 cells had elevated leukemia stem cell (LSC) levels. Gene expression microarray analysis revealed a panel of differential expressed genes including Sex-determining region Y (SRY)-box 13 (Sox13). Furthermore, a positive correlation between the expressions of IL-34 and Sox13 was detected human datasets. Knockdown of Sox13 rescued the enhanced proliferation, high LSC level and subcutaneous infiltration in MA9-IL-34 cells. Moreover, more leukemia-associated macrophages (LAMs) were detected in MA9-IL-34 microenvironment. Additionally, those LAMs showed M2-like phenotype since they expressed high level of M2-associated genes and had attenuated phagocytic potential, suggesting that LAMs should also contribute to IL-34 caused adverse phenotypes. Therefore, our findings uncover the intrinsic and microenvironmental mechanisms of IL-34 in AML and broadens the knowledge of M-CSF/IL-34-CSF-1R axis in malignancies.

show abstract

Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells

Cited by 9 publications

References 99 publications

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

microRNA expression in acute myeloid leukaemia: New targets for therapy?

Sox13 and M2-like leukemia-associated macrophages contribute to endogenous IL-34 caused accelerated progression of acute myeloid leukemia

Contact Info

Product

Resources

About