Correlation between SALL4 stemness marker and bone morphogenetic protein signaling genes in esophageal squamous cell carcinoma

Assarnia, Sogand; Khales, Sima Ardalan; Forghanifard, Mohammad Mahdi

doi:10.1002/jbt.22262

Cited by 7 publications

(7 citation statements)

References 17 publications

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“…Importantly, we demonstrated that the choriocarcinoma-associated transcription factor Sall4 was increased in situ in the postmolar choriocarcinoma cohort compared to that of the complete mole counterpart. This finding is in line with previous studies demonstrating that Sall4 plays a key role in tumorigenesis and tumor cell invasiveness through its correlation with TGF-β signaling genes [24,25].…”

Section: Discussionsupporting

confidence: 93%

Transcriptomic Characterization of Postmolar Gestational Choriocarcinoma

et al. 2021

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The human placenta shares properties with solid tumors, such as rapid growth, tissue invasion, cell migration, angiogenesis, and immune evasion. However, the mechanisms that drive the evolution from premalignant proliferative placental diseases—called hydatidiform moles—to their malignant counterparts, gestational choriocarcinoma, as well as the factors underlying the increased aggressiveness of choriocarcinoma arising after term delivery compared to those developing from hydatidiform moles, are unknown. Using a 730-gene panel covering 13 cancer-associated canonical pathways, we compared the transcriptomic profiles of complete moles to those of postmolar choriocarcinoma samples and those of postmolar to post-term delivery choriocarcinoma. We identified 33 genes differentially expressed between complete moles and postmolar choriocarcinoma, which revealed TGF-β pathway dysregulation. We found the strong expression of SALL4, an upstream regulator of TGF-β, in postmolar choriocarcinoma, compared to moles, in which its expression was almost null. Finally, there were no differentially expressed genes between postmolar and post-term delivery choriocarcinoma samples. To conclude, the TGF-β pathway appears to be a crucial step in the progression of placental malignancies. Further studies should investigate the value of TGF- β family members as biomarkers and new therapeutic targets.

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Section: Discussionsupporting

confidence: 93%

Transcriptomic Characterization of Postmolar Gestational Choriocarcinoma

et al. 2021

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“…SALL4 is a novel, sensitive, and specific marker for metastatic germ cell tumors and is particularly useful for detecting metastatic yolk sac tumors 60 . Also, SALL4 plays a role in the invasiveness of ESCC by regulating BMP signaling genes 54 . In summary, these findings indicate that SALL4 is highly expressed in various types of cancer, and interference with SALL4 expression could effectively inhibit cancer metastasis.…”

Section: The Oncogenic Roles Of Sall4 In Cancermentioning

confidence: 79%

“…Moreover, SALL4 regulates the proliferation, apoptosis, cell cycle, and clonogenicity of ESCC cells 38 . For instance, SALL4 regulates bone morphogenetic protein (BMP) signaling transcription factors, as well as its target gene death‐inducer obliterator 1 ( DIDO1), to maintain the balance between tumor cell proliferation and apoptosis during ESCC tumorigenesis 54 …”

Section: The Oncogenic Roles Of Sall4 In Cancermentioning

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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“…Several mutation-driver genes (Mut-driver-genes) have been characterized in cancer cells so far (e.g., KRAS , BRAF , MYC , TP53 ), however vsDPGs have gained attention in the process of carcinogenesis due to their tumorigenic potential [ 145 , 146 , 147 ]. VENTX and NANOG were found highly expressed in brain (glioma/glioblastoma) [ 148 , 149 , 150 ], pancreatic [ 151 , 152 , 153 ] renal [ 154 , 155 ], esophageal [ 156 , 157 ] and testicular cancers [ 28 , 158 , 159 ]. Interestingly, VENTX and NANOG share activity in hematopoiesis by repressing the genes responsible for terminal differentiation (e.g., TAL1 , KLF1 ) [ 160 , 161 ], as well as promoting leukemia [ 161 , 162 , 163 ].…”

Section: Developmental Potential Guardians In Human Diseasesmentioning

confidence: 99%

Vertebrate Cell Differentiation, Evolution, and Diseases: The Vertebrate-Specific Developmental Potential Guardians VENTX/NANOG and POU5/OCT4 Enter the Stage

Ducos

Bensimon

Scerbo

2022

Cells

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During vertebrate development, embryonic cells pass through a continuum of transitory pluripotent states that precede multi-lineage commitment and morphogenesis. Such states are referred to as “refractory/naïve” and “competent/formative” pluripotency. The molecular mechanisms maintaining refractory pluripotency or driving the transition to competent pluripotency, as well as the cues regulating multi-lineage commitment, are evolutionarily conserved. Vertebrate-specific “Developmental Potential Guardians” (vsDPGs; i.e., VENTX/NANOG, POU5/OCT4), together with MEK1 (MAP2K1), coordinate the pluripotency continuum, competence for multi-lineage commitment and morphogenesis in vivo. During neurulation, vsDPGs empower ectodermal cells of the neuro-epithelial border (NEB) with multipotency and ectomesenchyme potential through an “endogenous reprogramming” process, giving rise to the neural crest cells (NCCs). Furthermore, vsDPGs are expressed in undifferentiated-bipotent neuro-mesodermal progenitor cells (NMPs), which participate in posterior axis elongation and growth. Finally, vsDPGs are involved in carcinogenesis, whereby they confer selective advantage to cancer stem cells (CSCs) and therapeutic resistance. Intriguingly, the heterogenous distribution of vsDPGs in these cell types impact on cellular potential and features. Here, we summarize the findings about the role of vsDPGs during vertebrate development and their selective advantage in evolution. Our aim to present a holistic view regarding vsDPGs as facilitators of both cell plasticity/adaptability and morphological innovation/variation. Moreover, vsDPGs may also be at the heart of carcinogenesis by allowing malignant cells to escape from physiological constraints and surveillance mechanisms.

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Correlation between SALL4 stemness marker and bone morphogenetic protein signaling genes in esophageal squamous cell carcinoma

Cited by 7 publications

References 17 publications

Transcriptomic Characterization of Postmolar Gestational Choriocarcinoma

Transcriptomic Characterization of Postmolar Gestational Choriocarcinoma

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

Vertebrate Cell Differentiation, Evolution, and Diseases: The Vertebrate-Specific Developmental Potential Guardians VENTX/NANOG and POU5/OCT4 Enter the Stage

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