SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells

Wu, Feng; Jordan, Ashley; Kluz, Thomas; Shen, Steven S.; Sun, Hong; Cartularo, Laura; Costa, Max

doi:10.1016/j.taap.2016.01.008

Cited by 12 publications

(30 citation statements)

References 35 publications

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“…In line with the finding that SATB2 reduction eliminated the transformation properties of arsenic‐transformed cells, we investigated whether knocking down of SATB2 in normal BEAS‐2B cells prior to arsenic exposure would prevent arsenic‐induced cell transformation. Of note, under normal conditions, SATB2 is only weakly expressed in the lung, but not detectable in BEAS‐2B cells . We knocked down SATB2 in BEAS‐2B cells that do not express this gene, using stable shRNA transfection to prevent its expected increase in expression after exposure to arsenic.…”

Section: Resultsmentioning

confidence: 99%

“…Of note, under normal conditions, SATB2 is only weakly expressed in the lung, but not detectable in BEAS-2B cells. 26,55 We knocked down SATB2 in BEAS-2B cells that do not express this gene, using stable shRNA transfection to prevent its expected increase in expression after exposure to arsenic. SATB2 was stably knocked down in BEAS-2B cells using shRNA (BEAS-2B/SATB2 shRNA) and cells were treated with 2 μM of arsenic for six consecutive weeks.…”

Section: Satb2 Knockdown Prevents As-induced Transformation In Beasmentioning

confidence: 99%

“…In fact, microarray analysis suggests that SATB2 is the only gene found up regulated in all four heavy metal‐induced (arsenic, nickel, chromium, and vanadium) BEAS‐2B transformed cells . However, existing studies show that SATB2 can exert both oncogenic and tumor suppressive functions, depending on the type of tumor tissue, or cell line . Overall, the finding that SATB2 expression is induced by multiple heavy metals as well as its contrasting functions in different cancer tissues and cell lines lead to an examination of its role in arsenic‐induced BEAS‐2B cell transformation.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have linked the possible role of SATB2 in heavy metal-induced cell transformation. 25,26 In fact, microarray analysis suggests that SATB2 is the only gene found up regulated in all four heavy metal-induced (arsenic, nickel, chromium, and vanadium) BEAS-2B transformed cells. 25 However, existing studies show that SATB2 can exert both oncogenic and tumor suppressive functions, depending on the type of tumor tissue, or cell line.…”

mentioning

confidence: 99%

“…25 However, existing studies show that SATB2 can exert both oncogenic and tumor suppressive functions, depending on the type of tumor tissue, or cell line. 23,[26][27][28][29][30][31][32][33][34][35] Overall, the finding that SATB2 expression is induced by multiple heavy metals as well as its contrasting functions in different cancer tissues and cell lines lead to an examination of its role in arsenic-induced BEAS-2B cell transformation.…”

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confidence: 99%

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Role of miR‐31 and SATB2 in arsenic‐induced malignant BEAS‐2B cell transformation

Chen

Sun

et al. 2018

Molecular Carcinogenesis

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Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public health concerns. Today, approximately 200 million people around the globe are exposed to arsenic-contaminated drinking water at levels greater than the World Health Organization's recommended limit of 10 parts per billion. As a class I human carcinogen, arsenic exposure is known to elicit various cancers, including lung, skin, liver, and kidney. Current evidence suggests that arsenic is capable of inducing both genotoxic and cytotoxic injury, as well as activating epigenetic pathways to induce carcinogenesis. Our study identifies a novel pathway that is implicated in arsenic-induced carcinogenesis. Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2). Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression. As a direct downstream target of miR-31, SATB2 is a prominent transcription factor, and nuclear matrix binding protein implicated in many types of human diseases including lung cancer. Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease. Overexpression of SATB2 induces malignant transformation of human bronchial epithelial (BEAS-2B) cells indicating the importance of the expression of miR-31 in preventing carcinogenesis by suppressing SATB2 protein levels.

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Section: Resultsmentioning

confidence: 99%

Section: Satb2 Knockdown Prevents As-induced Transformation In Beasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Role of miR‐31 and SATB2 in arsenic‐induced malignant BEAS‐2B cell transformation

Chen

Sun

et al. 2018

Molecular Carcinogenesis

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Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control

2019

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The special AT-rich DNA binding protein (SATB2) is a nuclear matrix-associated protein and an important transcription factor for biological development, gene regulation and chromatin remodeling. Aberrant regulation of SATB2 has been found to highly correlate with various types of cancers including lung, colon, prostate, breast, gastric and liver. Recent studies have revealed that a subset of small non-coding RNAs, termed microRNAs (miRNAs), are important regulators of SATB2 function. As post-transcriptional regulators, miRNAs have been found to have fundament importance maintaining normal cellular development. Evidence suggests that multiple miRNAs, including miR-31, miR-34, miR-182, miR-211, miR-599, are capable of regulating SATB2 in cancers of the lung, liver, colon and breast. This review examines the molecular functions of SATB2 and miRNAs in the text of cancer development and potential strategies for cancer therapy with a focus on systemic miRNA delivery.

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SATB2 induction of a neural crest mesenchyme-like program drives invasion and drug resistance in melanoma

Fazio

Dang

et al. 2020

Preprint

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Recent genomic and scRNA-seq analyses of melanoma identified common transcriptional states correlating with invasion or drug resistance, but failed to find recurrent drivers of metastasis. To test whether transcriptional adaptation can drive melanoma progression, we made use of a zebrafish mitfa:BRAFV600E;tp53-/- model, in which malignant progression is characterized by minimal genetic evolution. We undertook an overexpression-screen of 80 epigenetic/transcriptional regulators and found neural crest-mesenchyme developmental regulator SATB2 to accelerate aggressive melanoma development. Its overexpression induces invadopodia formation and invasion in zebrafish tumors and human melanoma cell lines. SATB2 binds and activates neural crest-regulators, including pdgfab and snai2. The transcriptional program induced by SATB2 overlaps with known MITFlowAXLhigh and AQP1+NGFR1high drug resistant states and functionally drives enhanced tumor propagation and resistance to Vemurafenib in vivo. Here we show that melanoma transcriptional rewiring by SATB2 to a neural crest mesenchyme-like program can drive invasion and drug resistance in endogenous tumors.

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SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells

Cited by 12 publications

References 35 publications

Role of miR‐31 and SATB2 in arsenic‐induced malignant BEAS‐2B cell transformation

Role of miR‐31 and SATB2 in arsenic‐induced malignant BEAS‐2B cell transformation

Deregulation of SATB2 in carcinogenesis with emphasis on miRNA-mediated control

SATB2 induction of a neural crest mesenchyme-like program drives invasion and drug resistance in melanoma

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