Down-regulation of BORIS/CTCFL efficiently regulates cancer stemness and metastasis in MYCN amplified neuroblastoma cell line by modulating Wnt/β-catenin signaling pathway

Garikapati, Koteswara Rao; Patel, Nibedita; Makani, Venkata Krishna Kanth; Cilamkoti, Priyanka; Bhadra, Utpal; Bhadra, Manika Pal

doi:10.1016/j.bbrc.2017.01.066

Cited by 31 publications

(28 citation statements)

References 36 publications

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“…Our observation that BORIS-expressing melanoma cells have increased migratory and invasive abilities are in agreement with previous studies that demonstrated that BORIS overexpression promoted EMT in liver cancer cell lines (25) as well as the CD44/CD133 positive subpopulation of the IMR-32 neuroblastoma cell line (65). However, in contrast, Alberti et al, revealed that BORIS knockdown promotes EMT in MCF7 breast cancer cells (66).…”

Section: Discussionsupporting

confidence: 93%

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

Janssen

Moscona

Elchebly³

et al. 2019

Preprint

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Melanoma is among the most aggressive cancers due to its tendency to metastasize early. Phenotype switching between a proliferative and an invasive state has been suggested as a critical process for metastasis. The mechanisms that regulate these transitions are complex and remain poorly understood. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcriptional modulator that becomes aberrantly expressed in melanoma. Here, we show that BORIS is involved in phenotype switching in melanoma. Genetic modification of BORIS expression in melanoma cells combined with whole transcriptome analysis indicated that BORIS expression contributes to an invasion-associated transcriptome. In agreement with this finding, inducible BORIS overexpression in melanoma cells reduced proliferation and increased migration and invasion, demonstrating that the transcriptional switch is accompanied by a phenotypic switch. Overall, our study indicates a pro-invasive role for BORIS in melanoma via transcriptional reprogramming.

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Section: Discussionsupporting

confidence: 93%

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

Janssen

Moscona

Elchebly³

et al. 2019

Preprint

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“…Expression of BORIS has been found in some EC [ 30 , 43 ], and CSCs from neuroblastoma, cervical, colon and breast cancers [ 39 – 42 ]. In addition, expression of BORIS shows a positive correlation with specific stemness and CSC markers [ 40 , 43 , 44 ]. Thus, BORIS is considered to be a positive regulator of cancer/stem cell markers, and to have a role in the maintenance of CSC population in tumors [ 34 , 39 , 40 , 44 ].…”

Section: Boris In Cancer Stem Cellsmentioning

confidence: 99%

BORIS: a key regulator of cancer stemness

Soltanian

Dehghani

2018

Cancer Cell Int

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BORIS (CTCFL) is a DNA binding protein which is involved in tumorigenesis. Although, there are different opinions on the level of gene expression and function of BORIS in normal and cancer tissues, the results of many studies have classified BORIS as a protein belonging to cancer/testis (CT) genes, which are identified as a group of genes that are expressed normally in testis, and abnormally in various types of cancers. In testis, BORIS induces the expression of some male germ cell/testis specific genes, and plays crucial roles during spermatogenesis and production of sperm. In tumorigenesis, the role of BORIS in the expression induction of some CT genes and oncogenes, as well as increasing proliferation/viability of cancer cells has been demonstrated in many researches. In addition to cancer cells, some believe that BORIS is also expressed in normal conditions and plays a universal function in cell division and regulation of genes. The following is a comprehensive review on contradictory views on the expression pattern and biological function of BORIS in normal, as well as cancer cells/tissues, and presents some evidence that support the expression of BORIS in cancer stem cells (CSCs) and advanced stage/poorer differentiation grade of cancers. Boris is involved in the regulation of CSC cellular and molecular features such as self-renewal, chemo-resistance, tumorigenicity, sphere-forming ability, and migration capacity. Finally, the role of BORIS in regulating two important signaling pathways including Wnt/β-catenin and Notch in CSCs, and its ability in recruiting transcription factors or chromatin-remodeling proteins to induce tumorigenesis is discussed.

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“…TNC also plays an important role in promoting tumor stemness. For instance, Wnt/b-catenin signaling has an important role in regulating the balance between differentiation and stemness in a number of adult stem cell niches (33), and TNC modulates Wnt/ b-catenin signaling in glioma cells (27). In addition, TNC has been shown to elevate components of stem cell signaling, such as musashi homolog 1, a positive regulator of NOTCH signaling in breast cancer cells, thus linking TNC to NOTCH signaling pathway (34).…”

Section: Introductionmentioning

confidence: 99%

Activation of NOTCH Signaling by Tenascin-C Promotes Growth of Human Brain Tumor-Initiating Cells

et al. 2017

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Oncogenic signaling by NOTCH is elevated in brain tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is unknown. Here we provide evidence that tenascin-C (TNC), an extracellular matrix protein prominent in malignant glioma, increases NOTCH activity in BTIC to promote their growth. We demonstrate the proximal localization of TNC and BTIC in human glioblastoma specimens and in orthotopic murine xenografts of human BTIC implanted intracranially. In tissue culture, TNC was superior amongst several extracellular matrix proteins in enhancing the sphere-forming capacity of glioma patient-derived BTIC. Exogenously applied or autocrine TNC increased BTIC growth through an α2β1 integrin-mediated mechanism that elevated NOTCH ligand Jagged1 (JAG1). Microarray analyses and confirmatory PCR and Western analyses in BTIC determined that NOTCH signaling components including JAG1, ADAMTS15, and NICD1/2 were elevated in BITC after TNC exposure. Inhibition of γ-secretase and metalloproteinase proteolysis in the NOTCH pathway, or silencing of α2β1 integrin or JAG1, reduced the proliferative effect of TNC on BTIC. Collectively, our findings identified TNC as a pivotal initiator of elevated NOTCH signaling in BTIC and define the establishment of a TN-α2β1-JAG1-NOTCH signaling axis as a candidate therapeutic target in glioma patients. .

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Down-regulation of BORIS/CTCFL efficiently regulates cancer stemness and metastasis in MYCN amplified neuroblastoma cell line by modulating Wnt/β-catenin signaling pathway

Cited by 31 publications

References 36 publications

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

BORIS: a key regulator of cancer stemness

Activation of NOTCH Signaling by Tenascin-C Promotes Growth of Human Brain Tumor-Initiating Cells

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