The transcriptional activity of co‐activator AIB1 is regulated by the SUMO E3 Ligase PIAS1

Li, Shujing; Yang, Chunhua; Hong, Yongde; Bi, Hai-Lian; Zhao, Feng; Liu, Ying; Ao, Xiang; Pang, Pengsha; Xing, Xinrong; Chang, Alan K.; Xiao, Li; Zhang, Yuanyuan; Wu, Harry X.

doi:10.1111/boc.201100116

Cited by 20 publications

(20 citation statements)

References 38 publications

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“…We have previously shown that the AIB1 is required for breast cancer cell proliferation and demonstrated that its transcriptional activity is up-regulated by phosphorylation and down-regulated by sumoylation, and identified PIAS1 as the SUMO E3 ligase that can enhance the sumoylation of AIB1, thereby down-regulating AIB1 transcriptional activity [24], [25]. In this study, we used a combined molecular and cellular approach to characterize the role of AIB1 in EMT.…”

Section: Introductionmentioning

confidence: 99%

AIB1 Cooperates with ERα to Promote Epithelial Mesenchymal Transition in Breast Cancer through SNAI1 Activation

Wang

Zhao

et al. 2013

PLoS ONE

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Epithelial Mesenchymal Transition (EMT) plays a major role in cancer metastasis. Several genes have been shown to play a role in EMT, and one of these is Amplified-in-breast cancer 1 (AIB1), which has oncogenic function and is known to be amplified in breast cancer. However, the role of AIB1 in EMT remains largely undefined at the molecular level. In this study, the effect of AIB1 overexpression on the EMT of the breast cancer cell line T47D was investigated. Overexpression of AIB1 disrupted the epithelial morphology of the cells. At the same time, the cells displayed a strong metastasis and reduced level of the epithelial marker E-cadherin. In contrast, knockdown of AIB1 in T47D cells increased cell-cell adhesion and produced weak metastasis, as well as a higher level of E-cadherin expression. We proposed that the regulation of EMT by AIB1 occurred through the action of the transcription factor SNAI1, and demonstrated that such interaction required the participation of ERα and the presence of ERα-binding site on SNAI1 promoter. The expression level of E-cadherin and the extent of cell migration and invasion in SNAI1-knocked down T47D cells that overexpressed AIB1 were similar to those of T47D cells that did not overexpress AIB1 and had no SNAI1 knockdown. Taken together, these results suggested that AIB1 exerted its effect on EMT through its interaction with ERα, which could directly bind to the ERα-binding site on the SNAI1 promoter, allowing the AIB1-ERα complex to promote the transcription of SNAI1 and eventually led to repression of E-cadherin expression, consistent with the loss of E-cadherin being a hallmark of EMT.

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Section: Introductionmentioning

confidence: 99%

AIB1 Cooperates with ERα to Promote Epithelial Mesenchymal Transition in Breast Cancer through SNAI1 Activation

Wang

Zhao

et al. 2013

PLoS ONE

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“…In addition to SnoN, PIAS1 triggers sumoylation of other proteins including c-myc [42], Mdm2 [31] and AIB1 [43]. Thus, it would be interesting to evaluate the contribution of other PIAS1 SUMO substrates in its potential ability to regulate breast cancer invasiveness and metastasis, and to its utility as a biomarker in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of the SUMO E3 ligase PIAS1 as a potential survival biomarker in breast cancer

et al. 2017

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Metastasis is the ultimate cause of breast cancer related mortality. Epithelial-mesenchymal transition (EMT) is thought to play a crucial role in the metastatic potential of breast cancer. Growing evidence has implicated the SUMO E3 ligase PIAS1 in the regulation of EMT in mammary epithelial cells and breast cancer metastasis. However, the relevance of PIAS1 in human cancer and mechanisms by which PIAS1 might regulate breast cancer metastasis remain to be elucidated. Using tissue-microarray analysis (TMA), we report that the protein abundance and subcellular localization of PIAS1 correlate with disease specific overall survival of a cohort of breast cancer patients. In mechanistic studies, we find that PIAS1 acts via sumoylation of the transcriptional regulator SnoN to suppress invasive growth of MDA-MB-231 human breast cancer cell-derived organoids. Our studies thus identify the SUMO E3 ligase PIAS1 as a prognostic biomarker in breast cancer, and suggest a potential role for the PIAS1-SnoN sumoylation pathway in controlling breast cancer metastasis.

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“…Human breast cancer cell lines MCF-7, T47D, MCF10A and MDA-MB-231 have been used in our previous studies [31]–[34]. MCF-7 and MDA-MB-231 cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM) containing 10% fetal bovine serum (Hyclone, Logan, UT), 100 µg/ml penicillin and 100 µg/ml streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Induction of the CLOCK Gene by E2-ERα Signaling Promotes the Proliferation of Breast Cancer Cells

et al. 2014

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Growing genetic and epidemiological evidence suggests a direct connection between the disruption of circadian rhythm and breast cancer. Moreover, the expression of several molecular components constituting the circadian clock machinery has been found to be modulated by estrogen-estrogen receptor α (E2-ERα) signaling in ERα-positive breast cancer cells. In this study, we investigated the regulation of CLOCK expression by ERα and its roles in cell proliferation. Immunohistochemical analysis of human breast tumor samples revealed high expression of CLOCK in ERα-positive breast tumor samples. Subsequent experiments using ERα-positive human breast cancer cell lines showed that both protein and mRNA levels of CLOCK were up-regulated by E2 and ERα. In these cells, E2 promoted the binding of ERα to the EREs (estrogen-response elements) of CLOCK promoter, thereby up-regulating the transcription of CLOCK. Knockdown of CLOCK attenuated cell proliferation in ERα-positive breast cancer cells. Taken together, these results demonstrated that CLOCK could be an important gene that mediates cell proliferation in breast cancer cells.

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The transcriptional activity of co‐activator AIB1 is regulated by the SUMO E3 Ligase PIAS1

Abstract: Taken together, these results suggested that PIAS1 may play a crucial role in the regulation of AIB1 transcriptional activity through sumoylation.

Cited by 20 publications

References 38 publications

AIB1 Cooperates with ERα to Promote Epithelial Mesenchymal Transition in Breast Cancer through SNAI1 Activation

AIB1 Cooperates with ERα to Promote Epithelial Mesenchymal Transition in Breast Cancer through SNAI1 Activation

Identification of the SUMO E3 ligase PIAS1 as a potential survival biomarker in breast cancer

Induction of the CLOCK Gene by E2-ERα Signaling Promotes the Proliferation of Breast Cancer Cells

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