Silencing of bach1 gene by small interfering RNA–mediation regulates invasive and expression level of miR-203, miR-145, matrix metalloproteinase-9, and CXCR4 receptor in MDA-MB-468 breast cancer cells

Mohammadzadeh, Reza; Harouyan, Mojgan Saeid; Taha, Seyed Mansour Ale

doi:10.1177/1010428317695925

Cited by 12 publications

(7 citation statements)

References 34 publications

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“…An increasing number of studies have reported that miR‐203 is frequently downregulated in numerous types of cancer cells, such as osteosarcoma, colorectal cancer, hepatocellular carcinoma, breast cancer, and NSCLC cells. Changes in the expression of miR‐203 results in antitumor effects, suggesting that miR‐203 plays an important role in regulating tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

et al. 2017

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Involvement of the RGS17 oncogene in the promotion of non‐small‐cell lung cancer (NSCLC) has been reported, but the regulation mechanism in NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand the role of miRNAs in Regulator of G Protein Signaling 17 (RGS17)‐induced NSCLC, we showed that miR‐203 was downregulated during tumorigenesis, and inhibited the proliferation and invasion of lung cancer cells. We then determined whether miR‐203 regulated NSCLC by targeting RGS17. To characterize the regulatory effect of miR‐203 on RGS17, we used lung cancer cell lines, A549 and Calu‐1, and the constructed miR‐203 and RGS17 overexpression vectors. The CCK8 kit was used to determine cell proliferation, and the Transwell® assay was used to measure cell invasion and migration. RT‐PCR, western blots, and immunofluorescence were used to analyze expression of miR‐203 and RGS17, and the luciferase reporter assay was used to examine the interaction between miR‐203 and RGS17. Nude mice were used to characterize in vivo tumor growth regulation. Expression of miR‐203 inhibited proliferation, invasion, and migration of lung cancer cell lines A549 and Calu‐1 by targeting RGS17. The regulatory effect of miR‐203 was inhibited after overexpression of RGS17. The luciferase reporter assay showed that miR‐203 downregulated RGS17 by direct integration into the 3′‐UTR of RGS17 mRNA. In vivo studies showed that expression of miR‐203 significantly inhibited growth of tumors. Taken together, the results suggested that expression of miR‐203 inhibited tumor growth and metastasis by targeting RGS17.

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Section: Discussionmentioning

confidence: 99%

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

et al. 2017

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“…CXCR4 is known to increase cell migration ability and promote cancer metastasis ( 102 , 103 ). BACH1 has been reported to promote the expression of CXCR4 in colorectal ( 81 ) and breast cancers ( 75 , 99 , 104 ). However, no published study has examined whether or not BACH1 directly regulates CXCR4 .…”

Section: Functions Of Bach1 In Cancer Metastasismentioning

confidence: 99%

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

Igarashi

Nishizawa

Saiki

et al. 2021

Journal of Biological Chemistry

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The progression of cancer involves not only the gradual evolution of cells by mutations in DNA but also alterations in the gene expression induced by those mutations and input from the surrounding microenvironment. Such alterations contribute to cancer cells' abilities to reprogram metabolic pathways and undergo epithelial-to-mesenchymal transition (EMT), which facilitate the survival of cancer cells and their metastasis to other organs. Recently, BTB and CNC homology 1 (BACH1), a heme-regulated transcription factor that represses genes involved in iron and heme metabolism in normal cells, was shown to shape the metabolism and metastatic potential of cancer cells. The growing list of BACH1 target genes in cancer cells reveals that BACH1 promotes metastasis by regulating various sets of genes beyond iron metabolism. BACH1 represses the expression of genes that mediate cell–cell adhesion and oxidative phosphorylation but activates the expression of genes required for glycolysis, cell motility, and matrix protein degradation. Furthermore, BACH1 represses FOXA1 gene encoding an activator of epithelial genes and activates SNAI2 encoding a repressor of epithelial genes, forming a feedforward loop of EMT. By synthesizing these observations, we propose a “two-faced BACH1 model”, which accounts for the dynamic switching between metastasis and stress resistance along with cancer progression. We discuss here the possibility that BACH1-mediated promotion of cancer also brings increased sensitivity to iron-dependent cell death (ferroptosis) through crosstalk of BACH1 target genes, imposing programmed vulnerability upon cancer cells. We also discuss the future directions of this field, including the dynamics and plasticity of EMT.

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“…Other studies have demonstrated that common MMP-7 genetic polymorphisms are significant determinants of survival in Chinese patients with breast cancer (33). Overexpression of MMP-9 induced by the inflammatory cytokine interleukin-1β can promote MCF-7 cell metastasis, and the inhibition of MMP-9 can inhibit breast cancer cell metastasis (34)(35)(36)(37). Further studies indicated that MMP-9 is regulated by the NF-κB pathway, and that inhibition of MMP-9 via the NF-κB signaling pathway can suppress the MCF-7 cell invasion ability (38)(39)(40)(41).…”

Section: Bcsc-1 Immunostaining [N (%)] ------------------------------mentioning

confidence: 99%

BCSC-1 suppresses human breast cancer metastasis by inhibiting NF-κB signaling

Chen

Guo

et al. 2018

Int J Oncol

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Breast cancer suppressor candidate-1 (BCSC-1; also termed von Willebrand factor A domain containing 5A and LOH11CR2A) is a newly identified candidate tumor suppressor gene that has been implicated in several types of cancer in previous studies. However, there have been few reports about the association between BCSC-1 and human breast cancer in recent years. In the present study, the expression of BCSC-1 in breast cancer was determined by immunohistochemistry (IHC) staining of tissue microarrays and clinical tissue specimens. Subsequently, BCSC-1 gene expression was evaluated in different breast cancer cell lines by quantitative polymerase chain reaction and the MDA-MB-231 cell line was selected for further use in subsequent experiments, due to its low BCSC-1 expression. An MDA-MB-231 cell line with stable overexpression of BCSC-1 was established through transfection with plasmid containing the BCSC-1 gene, and then screening for G418 resistance. Wound-healing, migration and invasion assays were conducted to detect the effect of BCSC-1 on MDA-MB-231 cells. Furthermore, changes in matrix metalloproteinases (MMPs), osteopontin (OPN) and the nuclear factor-κB (NF-κB) pathway were detected in the current study. Additionally, stable silencing of BCSC-1 expression in MCF-7 cells was performed using a lentivirus. The results of IHC indicated that BCSC-1 is expressed at low levels in breast cancer tissues compared with in normal breast tissue. Results of the wound healing, migration and invasion assays demonstrated that BCSC-1 overexpression reduced the metastasis ability of MDA-MB-231 cells in vitro. Further research confirmed that the BCSC-1 overexpression reduced the expression levels of MMP7, MMP9 and OPN, and the phosphorylation of NF-κB p65. Furthermore, inhibition of BCSC-1 via lentivirus-mediated RNA interference revealed that the downregulation of BCSC-1 increased the invasive ability of MCF-7 cells. In summary, the results demonstrated that BCSC-1 is expressed at low levels in breast cancer tissues, and that it can suppress human breast cancer cell migration and invasion, potentially altering the expression of MMP7, MMP9, OPN, and the activity of the NF-κB pathway. Therefore, BCSC-1 may be useful as a biomarker for the treatment of breast cancer in the future.

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Silencing of bach1 gene by small interfering RNA–mediation regulates invasive and expression level of miR-203, miR-145, matrix metalloproteinase-9, and CXCR4 receptor in MDA-MB-468 breast cancer cells

Cited by 12 publications

References 34 publications

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

miR‐203 inhibits cell proliferation, invasion, and migration of non‐small‐cell lung cancer by downregulating RGS17

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis

BCSC-1 suppresses human breast cancer metastasis by inhibiting NF-κB signaling

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