SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation

Kanwore, Kouminin; Guo, Xinwen; Abdulrahman, Ayanlaja Abiola; Kambey, Piniel Alphayo; Nadeem, Iqra; Gao, Dianshuai

doi:10.1007/s12035-020-02240-6

Cited by 8 publications

(7 citation statements)

References 100 publications

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“…Group B of the SOX gene family consists of SOX1, SOX2, SOX3, SOX14, and SOX21. SOX1, SOX2, and SOX3 belong to subgroup B1, while SOX14 and SOX21 fall into subgroup B2 [77,[80][81][82].…”

Section: Group B (B1 + B2)mentioning

confidence: 99%

“…• Function: SOX1 plays a crucial role in maintaining stem cell lineage, particularly in embryogenesis, differentiation, and mammalian brain development. It is essential for the survival and function of dopaminergic neurons [80]; • Oncogenic properties: SOX1 has been implicated in the development of small cell lung, central nervous system, breast, and ovarian cancers. In small-cell lung cancer, SOX1 collaborates with NKX2.1 to maintain its identity and function.…”

Section: Sox1mentioning

confidence: 99%

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Clinical Significance of SOX10 Expression in Human Pathology

Bahmad,

Thiravialingam,

Sriganeshan

et al. 2023

CIMB

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The embryonic development of neural crest cells and subsequent tissue differentiation are intricately regulated by specific transcription factors. Among these, SOX10, a member of the SOX gene family, stands out. Located on chromosome 22q13, the SOX10 gene encodes a transcription factor crucial for the differentiation, migration, and maintenance of tissues derived from neural crest cells. It plays a pivotal role in developing various tissues, including the central and peripheral nervous systems, melanocytes, chondrocytes, and odontoblasts. Mutations in SOX10 have been associated with congenital disorders such as Waardenburg–Shah Syndrome, PCWH syndrome, and Kallman syndrome, underscoring its clinical significance. Furthermore, SOX10 is implicated in neural and neuroectodermal tumors, such as melanoma, malignant peripheral nerve sheath tumors (MPNSTs), and schwannomas, influencing processes like proliferation, migration, and differentiation. In mesenchymal tumors, SOX10 expression serves as a valuable marker for distinguishing between different tumor types. Additionally, SOX10 has been identified in various epithelial neoplasms, including breast, ovarian, salivary gland, nasopharyngeal, and bladder cancers, presenting itself as a potential diagnostic and prognostic marker. However, despite these associations, further research is imperative to elucidate its precise role in these malignancies.

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“…Group B of the SOX gene family consists of SOX1, SOX2, SOX3, SOX14, and SOX21. SOX1, SOX2, and SOX3 belong to subgroup B1, while SOX14 and SOX21 fall into subgroup B2 [77,[80][81][82].…”

Section: Group B (B1 + B2)mentioning

confidence: 99%

Section: Sox1mentioning

confidence: 99%

Clinical Significance of SOX10 Expression in Human Pathology

Bahmad,

Thiravialingam,

Sriganeshan

et al. 2023

CIMB

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“…SOX1 plays several roles in brain cancer, including proliferation, invasion, migration, and survival (Garcia et al, 2017). The diverging opinion on SOX1 gene is mainly due to its two genes on chromosome 13 and Y. SOX1 can revive the central nervous system dead neurons and prevent them from dying by regulating their electrical impulse (Kanwore et al, 2021). We also attribute this function to the mitochondria, which played a key role in electron transport, and metabolism within neurons to promote the survival of an isolated cell.…”

Section: Modification Of the Mitochondrial Metabolic Activity In A Single Isolated Cell Correlates With Oncogene Upregulation And Energy mentioning

confidence: 99%

Extracellular and Intracellular Factors in Brain Cancer

Kanwore

Kambey

Guo

et al. 2021

Front. Cell Dev. Biol.

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The external and internal factors of the cell are critical to glioma initiation. Several factors and molecules have been reported to be implicated in the initiation and progression of brain cancer. However, the exact sequence of events responsible for glioma initiation is still unknown. Existing reports indicate that glioma stem cells are the cell of glioma origin. During cell division, chromosome breakage, DNA alteration increases the chance of cell genome modifications and oncogene overexpression. Although there is a high risk of gene alteration and oncogene overexpression, not everyone develops cancer. During embryogenesis, the same oncogenes that promote cancers have also been reported to be highly expressed, but this high expression which does not lead to carcinogenesis raises questions about the role of oncogenes in carcinogenesis. The resistance of cancer cells to drugs, apoptosis, and immune cells does not rely solely on oncogene overexpression but also on the defect in cell organelle machinery (mitochondria, endoplasmic reticulum, and cytoskeleton). This review discusses factors contributing to cancer; we report the dysfunction of the cell organelles and their contribution to carcinogenesis, while oncogene overexpression promotes tumorigenesis, maintenance, and progression through cell adhesion. All these factors together represent a fundamental requirement for cancer and its development.

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“…Munkley J et al 2015 andMcHenry J et al 2014 demonstrated an interaction between SOX-1 and testosterone at mRNA level [7,8]. Kanwore K. et al 2020 reported a possible interaction between glial cell line-derived neurotrophic factor (GDNF) and SOX-1 that may regulate glioblastoma malignancy [9]. GDNF was first isolated in 1993 by Lin et al and shown to contribute to brain cancer development [10].…”

Section: Introductionmentioning

confidence: 99%

Testosterone upregulates glial cell line-derived neurotrophic factor (GDNF) and promotes neuroinflammation to enhance glioma cell survival and proliferation

Kanwore,

Guo

et al. 2023

Inflamm Regener

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Background Testosterone contributes to male organism development, such as bone density, muscle development, and fat repartition. Estrogen (derived from testosterone) also contributes to female reproductive system development. Here, we investigated the effect of testosterone on glioma cells and brain neuron inflammation essential for cancer development and progression. Methods The human astrocyte and glioma cell lines were treated with 6 ng/ml exogenous testosterone in vitro. We performed cell counting kit-8, transwell, and wound healing assays to determine the effect of testosterone on glioma cell proliferation, migration, and invasion. The glioma cells were injected into the xenograft and treated with 5 µl concentrated testosterone. Transcriptional suppression of glial cell line-derived neurotrophic factor (GDNF) was performed to evaluate brain neuron inflammation and survival. The tumor tissues were assessed by hematoxylin–eosin staining and immunohistochemistry. Results Testosterone upregulates GDNF to stimulate proliferation, migration, and invasion of glioma cells. Pathologically, the augmentation of GDNF and cyclophilin A contributed to neuroprotection when treated with testosterone. Our investigation showed that testosterone contributes to brain neuron and astrocyte inflammation through the upregulation of nuclear factor erythroid 2-related factor 2 (NRF2), glial fibrillary acid protein (GFAP), and sirtuin 5 (SIRT5), resulting in pro-inflammatory macrophages recruitments into the neural microenvironment. Mechanically, testosterone treatment regulates GDNF translocation from the glioma cells and astrocyte nuclei to the cytoplasm. Conclusion Testosterone upregulates GDNF in glioma cells and astrocytes essential for microglial proliferation, migration, and invasion. Testosterone contributes to brain tumor growth via GDNF and inflammation. Graphical Abstract The contribution of testosterone, macrophages, and astrocytes, in old neuron rescue, survival, and proliferation. During brain neuron inflammation, the organism activates and stimulates the neuron rescue through the enrichment of the old neuron microenvironment with growth factors such as GDNF, BDNF, SOX1/2, and MAPK secreted by the surrounding neurons and glial cells to maintain the damaged neuron by inflammation alive even if the axon is dead. The immune response also contributes to brain cell survival through the secretion of proinflammatory cytokines, resulting in inflammation maintenance. The rescued old neuron interaction with infiltrated macrophages contributes to angiogenesis to supplement the old neuron with more nutrients leading to metabolism activation and surrounding cell uncontrollable cell growth.

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SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation

Cited by 8 publications

References 100 publications

Clinical Significance of SOX10 Expression in Human Pathology

Clinical Significance of SOX10 Expression in Human Pathology

Extracellular and Intracellular Factors in Brain Cancer

Testosterone upregulates glial cell line-derived neurotrophic factor (GDNF) and promotes neuroinflammation to enhance glioma cell survival and proliferation

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