Transcription factors in SOX family: Potent regulators for cancer initiation and development in the human body

Kumar, Prasann; Mistri, Tapan Kumar

doi:10.1016/j.semcancer.2019.06.016

Cited by 61 publications

(23 citation statements)

References 144 publications

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“…SOX genes share a common HMG domain and all 20 family members are transcription factors that show greater than 60% similarity to the sex-determining region on the Y chromosome (SRY) gene. SOX genes have been shown to be able to act as both oncogenes and tumour suppressor genes in solid tumours (reviewed recently in [ 45 ]) and may also be involved in key pathogenetic pathways in AML involving CEBPA mutations, activation of β-catenin/Wnt and Hedgehog pathways and aberrant TP53 signals. We found SOX6 in both TCGA poor versus good and intermediate versus good risk subgroup comparisons and SOX5 , SOX15 and SOX18 in both the TARGET standard versus low risk and TCGA poor versus good risk subgroup comparisons; however, only SOX18 has previously been implicated in reduced disease-free and OS in AML patients [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Genes Whose Expression Overlaps Age Boundaries and Correlates with Risk Groups in Paediatric and Adult Acute Myeloid Leukaemia

Davis

Mills

Orchard

et al. 2020

Cancers

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Few studies have compared gene expression in paediatric and adult acute myeloid leukaemia (AML). In this study, we have analysed mRNA-sequencing data from two publicly accessible databases: (1) National Cancer Institute’s Therapeutically Applicable Research to Generate Effective Treatments (NCI-TARGET), examining paediatric patients, and (2) The Cancer Genome Atlas (TCGA), examining adult patients with AML. With a particular focus on 144 known tumour antigens, we identified STEAP1, SAGE1, MORC4, SLC34A2 and CEACAM3 as significantly different in their expression between standard and low risk paediatric AML patient subgroups, as well as between poor and good, and intermediate and good risk adult AML patient subgroups. We found significant differences in event-free survival (EFS) in paediatric AML patients, when comparing standard and low risk subgroups, and quartile expression levels of BIRC5, MAGEF1, MELTF, STEAP1 and VGLL4. We found significant differences in EFS in adult AML patients when comparing intermediate and good, and poor and good risk adult AML patient subgroups and quartile expression levels of MORC4 and SAGE1, respectively. When examining Kyoto Encyclopedia of Genes and Genomes (KEGG) (2016) pathway data, we found that genes altered in AML were involved in key processes such as the evasion of apoptosis (BIRC5, WNT1) or the control of cell proliferation (SSX2IP, AML1-ETO). For the first time we have compared gene expression in paediatric AML patients with that of adult AML patients. This study provides unique insights into the differences and similarities in the gene expression that underlies AML, the genes that are significantly differently expressed between risk subgroups, and provides new insights into the molecular pathways involved in AML pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Identification of Genes Whose Expression Overlaps Age Boundaries and Correlates with Risk Groups in Paediatric and Adult Acute Myeloid Leukaemia

Davis

Mills

Orchard

et al. 2020

Cancers

View full text Add to dashboard Cite

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“…43 Hence, we further explore the im- family, which encodes a transcription factor with a highly conserved high-mobility group (HMG) DNA-binding domain. 44 Previous reports have revealed that SOX5, SOX6, SOX9, SOX10 and SOX18 are all involved in the regulation of key melanocytic genes as transcription factors. [45][46][47][48] In particular, SOX9 has been demonstrated to play a key role in melanogenesis in adults, and SOX10 has been found to seriously influence the development of melanocytes.…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of exosomal miR‐200c derived from keratinocytes in vitiligo lesions suppresses melanogenesis

Zhao

Wang

et al. 2020

J Cellular Molecular Medi

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Vitiligo is an acquired disfiguring dermatosis characterized by patchy depigmentation due to the selective loss of functioning melanocytes. The incidence rate of vitiligo is approximately 0.5%-1.0% of the world's population. 1 At present, the aetiology of vitiligo remains unclear. Multiple studies demonstrated that massive oxidative stress may lead to vitiligo. Oxidation pathway is regarded as the important steps in the development of vitiligo. 2 In human skin, each melanocyte forms an epidermal melanin unit with 36 keratinocytes, which play an important role in maintaining melanocyte homeostasis. 3 Various growth factors produced by keratinocytes affect melanocyte proliferation and differentiation, such as endothelin-1, stem cell factor and basic fibroblast growth factor. 4-6 Additionally, keratinocyte-derived soluble factors regulate the melanogenesis of neighbouring melanocytes. 7 Moreover, various hormonal and peptide factors produced

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“…An increasing number of studies have revealed the crucial regulatory roles of TFs in the manipulation of tumor-specific, addictive transcripts or cancer-related pathways, thus triggering carcinogenesis and promoting cancer development (16,17). However, the complete function and clinical significance of TFs in GC remains unclear.…”

Section: Discussionmentioning

confidence: 99%

PLXNC1 Enhances Carcinogenesis Through Transcriptional Activation of IL6ST in Gastric Cancer

et al. 2020

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Background: Transcriptional factors (TFs) are responsible for orchestrating gene transcription during cancer progression. However, their roles in gastric cancer (GC) remain unclear.Methods: We analyzed the differential expressions of TFs and, using GC cells and tissues, investigated plexin C1 (PLXNC1) RNA levels, as well as PLXNC1's clinical relevance and functional mechanisms. The molecular function of PLXNC1 was evaluated in vitro and in vivo. Kaplan-Meier curves and the log-rank test were used to analyze overall survival (OS) and disease-free survival (DFS).Results: PLXNC1 was frequently up-regulated in GC and associated with poor prognosis. The expression level of PLXNC1 could serve as an independent biomarker to predict a patient's overall survival. Notably, knockdown of PLXNC1 significantly abolished GC cell proliferation, and migration, and overexpression of PLXNC1 accelerated carcinogenesis in GC. The gene set enrichment analysis (GSEA) indicated that high-expression of PLXNC1 was positively correlated with the activation of epithelial-mesenchymal transition (EMT), TNF-α, and IL-6/STAT3 signaling pathways. PLXNC1 promoted proliferation and migration of GC cells through transcriptional activation of the interleukin 6 signal transducer (IL6ST), which could rescue the malignant behavior of PLXNC1-deficient GC cells. Conclusions:Our study demonstrated that the PLXNC1 plays an oncogenic role in GC patients. The PLXNC1-IL6ST axis represents a novel potential therapeutic target for GC.

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Transcription factors in SOX family: Potent regulators for cancer initiation and development in the human body

Cited by 61 publications

References 144 publications

Identification of Genes Whose Expression Overlaps Age Boundaries and Correlates with Risk Groups in Paediatric and Adult Acute Myeloid Leukaemia

Identification of Genes Whose Expression Overlaps Age Boundaries and Correlates with Risk Groups in Paediatric and Adult Acute Myeloid Leukaemia

Down‐regulation of exosomal miR‐200c derived from keratinocytes in vitiligo lesions suppresses melanogenesis

PLXNC1 Enhances Carcinogenesis Through Transcriptional Activation of IL6ST in Gastric Cancer

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