BACH1 silencing by siRNA inhibits migration of HT-29 colon cancer cells through reduction of metastasis-related genes

Davudian, Sadaf; Shajari, Neda; Kazemi, Tohid; Mansoori, Behzad; Salehi, Shima; Mohammadi, Ali; Shanehbandi, Dariush; Khaze, Vahid; Asadi, Milad; Baradaran, Behzad

doi:10.1016/j.biopha.2016.09.021

Cited by 55 publications

(38 citation statements)

References 45 publications

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“…Accumulating data establish BACH1 as a critical facilitator of tumorigenesis and metastasis in breast (Lee et al, 2013), colon (Davudian et al, 2016b), prostate (Shajari et al, 2018) ovarian (Han et al, 2019), and lung (Lignitto et al, 2019;Wiel et al, 2019) cancer. Elevated levels of BACH1 expression have been linked to a higher risk of breast cancer recurrence in patients (Liang et al, 2012), whereas association with metastatic spread and poorer prognosis has recently been suggested in the case of human ovarian cancer (Han et al, 2019) and lung adenocarcinoma (Lignitto et al, 2019;Wiel et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Inactivation of Raf kinase inhibitory protein during tumor expansion results in higher expression of BACH1 and its target genes C-X-C chemokine receptor type 4 (CXCR-4) and matrix metal-loproteinase1 (MMP1), established drivers of tumor progression and metastasis (Foley & Kuliopulos, 2014;Mishan et al, 2016). Furthermore, ablation of BACH1 in human colon carcinoma (Davudian et al, 2016b) or in prostate cancer cells (Shajari et al, 2018) prevents cell growth, migration, and invasion in vitro, decreasing the expression of its main metastasisrelated genes, MMP1, let-7a, and CXCR4. Interestingly, cxcr4 is expressed in the somites and the endothelium of zebrafish embryos (Chong et al, 2001), where we detect the expression of both bach2a and bach2b transcripts.…”

Section: Discussionmentioning

confidence: 99%

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BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression

Cohen¹,

Tempelhof²,

Raz

et al. 2020

Life Sci. Alliance

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Angiogenesis and lymphangiogenesis are key processes during embryogenesis as well as under physiological and pathological conditions. Vascular endothelial growth factor C (VEGFC), the ligand for both VEGFR2 and VEGFR3, is a central lymphangiogenic regulator that also drives angiogenesis. Here, we report that members of the highly conserved BACH (BTB and CNC homology) family of transcription factors regulate VEGFC expression, through direct binding to its promoter. Accordingly, down-regulation of bach2a hinders blood vessel formation and impairs lymphatic sprouting in a Vegfc-dependent manner during zebrafish embryonic development. In contrast, BACH1 overexpression enhances intratumoral blood vessel density and peritumoral lymphatic vessel diameter in ovarian and lung mouse tumor models. The effects on the vascular compartment correlate spatially and temporally with BACH1 transcriptional regulation of VEGFC expression. Altogether, our results uncover a novel role for the BACH/VEGFC signaling axis in lymphatic formation during embryogenesis and cancer, providing a novel potential target for therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression

Cohen¹,

Tempelhof²,

Raz

et al. 2020

Life Sci. Alliance

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“…Bach1 depletion had no effect on the growth of breast cancer cells in culture or on primary tumor growth in mice [ 48 ]; however, the expression of Bach1 and its target genes has been linked to a higher risk of breast cancer recurrence in patients [ 49 ], as well as increases in cell invasion and migration of prostate and colon cancer cells [ 50 – 52 ], while lower Bach1 levels have been associated with declines in breast tumor metastasis [ 48 ]. The prometastatic activity of Bach1 is at least partially mediated by increases in the expression of metastatic genes such as CXC-chemokine receptor 4 (CXCR4), high-mobility group AT-hook 2 (HMGA2), vimentin, and matrix metalloproteinases (MMPs) 1, 9, and 13 [ 51 , 52 ]. Furthermore, Bach1 both suppresses and is suppressed by the metastasis-suppressor Raf kinase inhibitory protein (RKIP), and computational models suggest that this interplay between Bach1 and RKIP, as well as their downstream targets, could provide a mechanism by which environmental factors and stochastic fluctuations can trigger a metastatic phenotype in previously noninvasive cells without altering the cells' genomes [ 53 ].…”

Section: Bach1 In Cancermentioning

confidence: 99%

Bach1: Function, Regulation, and Involvement in Disease

Zhang

Guo

Wei

et al. 2018

Oxidative Medicine and Cellular Longevity

125

114

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The transcription factor BTB and CNC homology 1 (Bach1) is widely expressed in most mammalian tissues and functions primarily as a transcriptional suppressor by heterodimerizing with small Maf proteins and binding to Maf recognition elements in the promoters of targeted genes. It has a key regulatory role in the production of reactive oxygen species, cell cycle, heme homeostasis, hematopoiesis, and immunity and has been shown to suppress ischemic angiogenesis and promote breast cancer metastasis. This review summarizes how Bach1 controls these and other cellular and physiological and pathological processes. Bach1 expression and function differ between different cell types. Thus, therapies designed to manipulate Bach1 expression will need to be tightly controlled and tailored for each specific disease state or cell type.

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“…al. [55] results indicated that BACH1 down-regulation in HT29 CRC cells had no effect on cell growth, however; they inhibited cell migration by decreasing metastasis-related gene expression. These results suggested that BACH1 may function as an oncogenic driver in colon cancer and may represent a potential target for gene therapy for colorectal cancer treatment.…”

Section: Gene Therapymentioning

confidence: 83%

Colorectal Cancer from Molecular Pathways to Gene Therapy

Kosmıdis¹,

Efthimidis²,

Baka³

et al. 2017

Oncomedicine

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Nowadays colorectal cancer is still considered the third most common cancer in the world. The tumorigenesis mechanisms of colorectal cancer have been widely studied at a molecular level. It has been observed that morbidity and mortality caused by colorectal cancer impacts on the global economy. This occurs through the loss of productivity and the burden on the healthcare system. Therefore an effort is made by several researchers to expend considerably their resources to develop treatments and preventative strategies to reduce the incidence of colorectal cancer. A Large-scale sequencing of genome, proteome, microbiome, and transcriptome analyses of colorectal cancer tissue has allowed researchers to better understand colorectal cancer subtypes. Until now the following parameters have been identified with the etiology of colorectal cancer genetic mutations, inflammatory processes, diet, and the gut microbes. In the current review we will present the molecular pathways of CRC and discuss novel gene therapy approaches.

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BACH1 silencing by siRNA inhibits migration of HT-29 colon cancer cells through reduction of metastasis-related genes

Cited by 55 publications

References 45 publications

BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression

BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression

Bach1: Function, Regulation, and Involvement in Disease

Colorectal Cancer from Molecular Pathways to Gene Therapy

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