SALL4 Gene Expression in Acute Myeloid Leukemia

Ibraheem, Fatma Mahmoud; Badawy, Rgia; Ayoub, M. M.; Hassan, Noha; Mostafa, Marwa Nabil

doi:10.31557/apjcp.2019.20.10.3121

Cited by 4 publications

(6 citation statements)

References 19 publications

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“…AML has a poor prognosis [183] and is a clonal disorder arising from the differentiation arrest of myeloid precursors and the malignant proliferation of bone marrow-derived, self-renewing stem or progenitor cells in the BM and blood [184]. Clinical sequelae generally include discomfort and fatigue, infection, bleeding and/or bruises, and often bone pain [185].…”

Section: Normal Hematopoietic Function and Leukemiamentioning

confidence: 99%

“…In the process of normal hematopoiesis, SALL4 is preferentially expressed in human CD34positive hematopoietic stem/progenitors and downregulated in CD34-negative cells during hematopoietic differentiation [33]. Aberrantly, SALL4 was expressed in primary leukemia, AML, and precursor B-cell lymphoblastic leukemia [184]. Furthermore, SALL4 expression correlates with disease progression in human CML, and its expression in AML patients correlates with treatment status [190].…”

Section: Normal Hematopoietic Function and Leukemiamentioning

confidence: 99%

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SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

Sun

et al. 2022

IJMS

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SALL4, a member of the SALL family, is an embryonic stem cell regulator involved in self-renewal and pluripotency. Recently, SALL4 overexpression was found in malignant cancers, including lung cancer, hepatocellular carcinoma, breast cancer, gastric cancer, colorectal cancer, osteosarcoma, acute myeloid leukemia, ovarian cancer, and glioma. This review updates recent advances of our knowledge of the biology of SALL4 with a focus on its mechanisms and regulatory functions in tumors and human hematopoiesis. SALL4 overexpression promotes proliferation, development, invasion, and migration in cancers through activation of the Wnt/β-catenin, PI3K/AKT, and Notch signaling pathways; expression of mitochondrial oxidative phosphorylation genes; and inhibition of the expression of the Bcl-2 family, caspase-related proteins, and death receptors. Additionally, SALL4 regulates tumor progression correlated with the immune microenvironment involved in the TNF family and gene expression through epigenetic mechanisms, consequently affecting hematopoiesis. Therefore, SALL4 plays a critical oncogenic role in gene transcription and tumor growth. However, there are still some scientific hypotheses to be tested regarding whether SALL4 is a therapeutic target, such as different tumor microenvironments and drug resistance. Thus, an in-depth understanding and study of the functions and mechanisms of SALL4 in cancer may help develop novel strategies for cancer therapy.

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Section: Normal Hematopoietic Function and Leukemiamentioning

confidence: 99%

Section: Normal Hematopoietic Function and Leukemiamentioning

confidence: 99%

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

Sun

et al. 2022

IJMS

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“…Previous studies on AML have mainly focused on mutant genes, namely, FLT3 , IDH2 , NPM1 , RUNX1 , TP53, and DNMT3A ( Ofran, 2014 ; Sudhindra and Smith, 2014 ; Ohgami et al, 2015 ; Papaemmanuil et al, 2016 ), miRNA ( Ali Syeda et al, 2020 ) and mRNA ( Blagden and Willis, 2011 ). Researchers have extensively investigated the expression patterns of mRNAs and miRNAs, and many mRNAs or miRNAs have been identified as prognostic markers for patients with AML ( Ge et al, 2019 ; Ibraheem et al, 2019 ; Elsayed et al, 2020 ). In recent years, a new class of noncoding RNA (lncRNA) has gradually become a research hotspot in various cancer fields ( Ferrè et al, 2016 ; Paraskevopoulou and Hatzigeorgiou, 2016 ; Qian et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

DesA Prognostic Risk Model of LncRNAs in Patients With Acute Myeloid Leukaemia Based on TCGA Data

Ding

Ling

Shi

et al. 2022

Front. Bioeng. Biotechnol.

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Purpose: This study aimed to combine the clinical data of acute myeloid leukaemia (AML) from The Cancer Genome Atlas (TCGA) database to obtain prognosis-related biomarkers, construct a prognostic risk model using long non-coding RNAs (lncRNAs) in AML and help patients with AML make clinical treatment decisions.Methods: We analysed the transcriptional group information of 151 patients with AML obtained from TCGA and extracted the expressions of lncRNAs. According to the mutation frequency, the patients were divided into the high mutation group (genomic unstable group, top 25% of mutation frequency) and low mutation group (genomic stable group, 25% after mutation frequency). The ‘limma’ R package was used to analyse the difference in lncRNA expressions between the two groups, and the “survival,” “caret,” and “glmnet” R packages were used to screen lncRNAs that are related to clinical prognosis. Subsequently, a prognosis-related risk model was constructed and verified through different methods.Results: According to the lncRNA expression data in TCGA, we found that seven lncRNAs (i.e. AL645608.6, LINC01436, AL645608.2, AC073534.2, LINC02593, AL512413.1, and AL645608.4) were highly correlated with the clinical prognosis of patients with AML, so we constructed a prognostic risk model of lncRNAs based on LINC01436, AC073534.2, and LINC02593. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses of differentially expressed lncRNA-related target genes were performed, receiver operating characteristic (ROC) curves were created, the applicability of the model in children was assessed using the TARGET database and the model was externally verified using the GEO database. Furthermore, different expression patterns of lncRNAs were validated in various AML cell lines derived from Homo sapiens.Conclusions: We have established a lncRNA prognostic model that can predict the survival of patients with AML. The Kaplan-Meier analysis showed that this model distinguished survival differences between patients with high- and low-risk status. The ROC analysis confirmed this finding and showed that the model had high prediction accuracy. The Kaplan-Meier analysis of the clinical subgroups showed that this model can predict prognosis independent of clinicopathological factors. Therefore, the proposed prognostic lncRNA risk model can be used as an independent biomarker of AML.

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“…SALL4 is one of the few genes in AML that connects the self‐renewal properties of ESCs, normal HSCs, and leukemia stem cells (LSCs). SALL4 gene expression is higher in AML patient samples than in controls 32 . Another study shows that AML patients who respond to treatment have lower SALL4 expression throughout the treatment course, whereas AML patients who have disease relapse or drug resistance have higher SALL4 expression 25 .…”

Section: Sall4 and Cancer Diagnosismentioning

confidence: 97%

“…This side population is involved in cancer initiation and drug resistance, and it is used to isolate cancer-initiating cells. 25 During leukemogenesis, SALL4 is expressed in myelodysplastic syndrome (MDS), 31 AML, 20,32 CML, 21 and precursor B-ALL. 22,23 In human AMLs, SALL4 knockdown results in massive cellular apoptosis and cell growth arrest, accounting for 91% of identified promoters that are considered genuine SALL4-binding loci in AML cells.…”

Section: Sall4 In Carcinogenesismentioning

confidence: 99%

The new advance of SALL4 in cancer: Function, regulation, and implication

Abouelnazar

Zhang

Wang

et al. 2023

Clinical Laboratory Analysis

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SALL4 (split-like protein 4) is a member of the mammalian homologs of the Drosophila homoeotic gene spalt (sal) and acts as a zinc finger transcription factor to govern the self-renewal and pluripotency of embryonic stem cells. SALL4 expression gradually decreases during development and is even absent in most adult tissues. However, increasing evidence suggests that SALL4 expression is restored in human cancers and its aberrant expression is associated with the progression of many hematopoietic malignancies and solid tumors. The potent roles of SALL4 in regulating cancer cell proliferation, apoptosis, metastasis, and drug resistance have been reported. SALL4 plays a dual role in epigenetic modulation by acting as either an activator or a repressor of its target genes. Furthermore, SALL4 interacts with other partners to control the expression of many downstream genes and the activation of various key signaling transduction pathways. SALL4 is considered as a promising diagnostic and prognostic biomarker and therapeutic target for cancer. In this review, we highlighted the major advances in the roles and mechanisms of SALL4 in cancer and the therapeutic strategies for targeting SALL4 to treat cancer.

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SALL4 Gene Expression in Acute Myeloid Leukemia

Abstract: SALL4 (sal-like protein 4) is a newly identified zinc-finger transcription factor and it is one of the SALL gene family (SALL1 to SALL4). It was cloned according to its sequence homology to Drosophila spalt (sal). Alternative splicing generates two variant forms of human

Cited by 4 publications

References 19 publications

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

DesA Prognostic Risk Model of LncRNAs in Patients With Acute Myeloid Leukaemia Based on TCGA Data

The new advance of SALL4 in cancer: Function, regulation, and implication

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