Silencing of BACH1 inhibits invasion and migration of prostate cancer cells by altering metastasis-related gene expression

Shajari, Neda; Davudian, Sadaf; Kazemi, Tohid; Mansoori, Behzad; Salehi, Shima; Khaze, Vahid; Shanehbandi, Dariush; Mohammadi, Ali; Duijf, Pascal H.G.; Baradaran, Behzad

doi:10.1080/21691401.2017.1374284

Cited by 49 publications

(45 citation statements)

References 31 publications

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“…CXCR4: C-X-C chemokine receptor type 4; miR: microRNA; MMP9: matrix metalloproteinase-9; VEGFR: vascular endothelial growth factor receptor [Color figure can be viewed at wileyonlinelibrary.com] expression ( Figure 7). These results are consistent with our previous results which were reached by specific silencing of Bach-1 (Shajari et al, 2018). In line with our present results and previous results, we suggested that miR-142-3p might regulate the expression of CXCR4, MMP9, and VEGFR through silencing of Bach-1 mRNA.…”

Section: The Mir-142-3p Mimic Sequence Could Increase the Level Of supporting

confidence: 94%

miR‐142‐3p as tumor suppressor miRNA in the regulation of tumorigenicity, invasion and migration of human breast cancer by targeting Bach‐1 expression

Mansoori

Mohammadi

Ghasabi

et al. 2018

Journal Cellular Physiology

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107

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Background Breast cancer is the most common type of cancer among women, and despite improved treatments, it remains a major challenge. However, improved mechanistic insight may lead to novel therapeutic strategies. miR‐142‐3p belongs to the miR‐142 family and is involved in pathogenesis and metastasis of various types of malignancies by targeting several important messenger RNAs (mRNAs) including Bach‐1. This is especially true for breast cancer, where Bach‐1 is involved in the metastatic spread by deregulation of metastasis‐associated genes. Methods In this study, we collected 24 breast cancer tissues with 24 adjusted normal tissues to measure the expression levels of miR‐142‐3p and Bach‐1 mRNA using quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) and IHC. miR‐142‐3p targeting of Bach‐1 expression in MCF‐7 and MDA‐MB‐468 breast cancer cells was evaluated using bioinformatics, qRT‐PCR and western blot analyses. The cellular proliferation, invasion, and migration were assessed by MTT, transwell matrigel and wound healing assay and the EMT‐associated proteins C‐X‐C chemokine receptor type 4 (CXCR‐4), matrix metalloproteinase‐9 (MMP9), and vascular endothelial growth factor receptor (VEGFR) were analyzed by western blot analysis. Also, the expression levels of tumor suppressors including miR‐330, miR‐145, and miR‐34a were estimated by qRT‐PCR. Results Analysis of paired specimens of primary malignant and normal tissues showed that miR‐142‐3p was downregulated, while Bach‐1 mRNA and protein both were overexpressed in the breast cancer tumors. This inverse relationship was confirmed by cell line experiments demonstrating that miR‐142‐3p expression reduced Bach‐1 mRNA levels. Furthermore, replacement of miR‐142‐3p could inhibit the proliferation, invasion, and migration in breast cancer potentially by targeting of Bach‐1 mRNA and subsequent inhibition of CXCR4, MMP9, and VEGFR protein expressions. In addition, induction of miR‐142‐3p could upregulate tumor suppressor miRNAs, including miR‐330, miR‐145, and miR34a. Conclusion For the first time, our results revealed that miR‐142‐3p could target Bach‐1in breast cancer cells leading to the reduction of EMT‐related proteins and reduced cell proliferation, invasion, and migration. The results also demonstrated that miR‐142‐3p could regulate important tumor suppressor miRNAs in breast cancer cells. In conclusion, our results suggest that miR‐142‐3p could be a good candidate for the targeted therapy of breast cancer, especially for the invasive type.

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Section: The Mir-142-3p Mimic Sequence Could Increase the Level Of supporting

confidence: 94%

miR‐142‐3p as tumor suppressor miRNA in the regulation of tumorigenicity, invasion and migration of human breast cancer by targeting Bach‐1 expression

Mansoori

Mohammadi

Ghasabi

et al. 2018

Journal Cellular Physiology

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107

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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%

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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“…These results support the hypothesis that miR-135a is involved in CC progression, which may function as an oncogenic factor. BACH1, a member of the basic leucine zipper transcription factor family, is a critical participant in the regulation of oxidative stress [24] .Recent researches demonstrated that BACH1 is a widely expressed transcriptional repressor, which takes part in cell cycle progression, apoptosis, and the hypoxia response negatively through the targeted genes [25][26][27][28] .As one of them, heme-oxygenase-1 (HO-1) might be significant in induction of the tumorigenic pathway. The expression of HO-1 increases significantly in various types of cancer, which is proved to promote tumor growth and metastasis and suppress the apoptosis of tumor cells.…”

Section: Resultsmentioning

confidence: 99%

The expression and Clinical Significance of miRNA-135a and Bach1 in colorectal cancer

Wang

Zhang

Jiang

et al. 2019

Preprint

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BACKGROUND AIM To explore the correlation between the expression of miRNA-135a and Bach1 in colorectal cancer tissue and the patient's clinical information. Methods 60 patients with colorectal carcinoma were treated as a control group. Real-time quantitative PCR assays and immunohistochemistry method were performed to detect the expression of miRNA-135a and bach1 in 50 colorectal carcinoma and adjacent normal tissues, and the clinical and pathological classifications have also been investigated. The SPSS 19.00 software was used. All data represent mean±SD of three independent experiments. P<0.05 was considered statistically significant. Results miRNA-135a expression levels increase significantly in the colon cancer tissues compared with the non-tumor control tissues(P<0.01). miRNA-135a expression levels are higher in stage III/IV than in stage I/II colon cancer patients. The expression level of Bach1 in colorectal cancer was significantly lower(P<0.01). Bach1 and mirna-135a are negatively correlated. Conclusions: mirna-135a and bach1 showed a negative correlation, it may be one of the important indices for colorectal cancer screening.

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Silencing of BACH1 inhibits invasion and migration of prostate cancer cells by altering metastasis-related gene expression

Cited by 49 publications

References 31 publications

miR‐142‐3p as tumor suppressor miRNA in the regulation of tumorigenicity, invasion and migration of human breast cancer by targeting Bach‐1 expression

miR‐142‐3p as tumor suppressor miRNA in the regulation of tumorigenicity, invasion and migration of human breast cancer by targeting Bach‐1 expression

BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression

The expression and Clinical Significance of miRNA-135a and Bach1 in colorectal cancer

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