Inhibitory effect of acetyl-11-keto-β-boswellic acid on androgen receptor by interference of Sp1 binding activity in prostate cancer cells

Yuan, Huipin; Kong, Feng; Wang, Xiaoling; Young, Charles Y.F.; Hu, Xiaoyan; Lou, Hongxiang

doi:10.1016/j.bcp.2008.03.005

Cited by 64 publications

(28 citation statements)

References 27 publications

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“…The anti-proliferative effects of AKBA were associated with reduction in AR transcript and protein [92]. Using reporter gene constructs and gel shift assays it was shown that the downregulation of AR was a result of the inhibition of Sp1 DNA binding activity by AKBA.…”

Section: Akbamentioning

confidence: 98%

Targeting SP1 Transcription Factor in Prostate Cancer Therapy

et al. 2011

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Transcription factors are proteins that regulate gene expression by binding to specific DNA sequences within gene promoter regions. Specificity protein (Sp) family transcription factors play a critical role in various cellular processes and have been shown to be associated with tumorigenesis. The Sp family consists of several members that contain a highly conserved DNA-binding domain composed of three zinc fingers at the C-terminus and serine/threonine- and glutamine-rich transactivation domains at the N-terminal. Sp1 is elevated in several cancers including prostate and is associated with the prognosis of patients. Sp1, Sp3, and Sp4 regulate a variety of cancer associated genes that are involved in cell cycle, proliferation, cell differentiation, and apoptosis. Studies have shown that in prostate cancer, Sp1 regulates important genes like androgen receptor, TGF-β, c-Met, fatty acid synthase, matrix metalloprotein (MT1-MMP), PSA, and α-integrin. These results highlight the importance of Sp1 in prostate cancer and emphasize the potential therapeutic value of targeting Sp1. Several strategies, including the use of natural and synthetic compounds, have been used to inhibit Sp1 in prostate cancer. These include polyphenol quercetin, betulinic acid, acetyl-11-keto-beta-boswellic acid, tea phenols, isothiocyanates, thiazolidinediones, arsenic trioxide, and selenium. This review will describe the association of Sp proteins in prostate cancer with a special emphasis on some of the agents tested to target Sp proteins for the treatment of this malignancy.

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Section: Akbamentioning

confidence: 98%

Targeting SP1 Transcription Factor in Prostate Cancer Therapy

et al. 2011

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“…It also decreased androgen receptor expression at mRNA and protein levels. Furthermore, evaluation of functional biomarkers showed suppressions of prostate-specific antigen promoter-dependent and androgen responsive element-dependent luciferase activities (Yuan et al, 2008).…”

Section: Prostate Cancermentioning

confidence: 99%

Pharmacological evidences for cytotoxic and antitumor properties of Boswellic acids from Boswellia serrata

Khan

Ali

Parveen

et al. 2016

Journal of Ethnopharmacology

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“…Given the important function of transcription factors in neoplastic mechanism, including apoptosis, angiogenesis, and metastasis (Xie et al 2006), characterization of their interaction with PTTG requires further investigation. Recent studies of Sp1 inhibition have shown promising anti-angiogenic and anti-fibrotic effects in prostate cancer as well as in kidney and lung fibrosis respectively (Chae et al 2006, Yuan et al 2008. Thus, the effects of Sp1 inhibition in neoplasms overexpressing PTTG should be investigated and may provide a potential therapeutic target in these neoplasms.…”

Section: Sp1mentioning

confidence: 99%

Pituitary tumor-transforming gene in endocrine and other neoplasms: a review and update

Salehi

Kovács²,

Scheithauer³

et al. 2008

Endocrine Related Cancer

118

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Pituitary tumor-transforming gene (PTTG) was only recently discovered. Its overexpression occurs in a wide variety of endocrine and non-endocrine tumors, including ones of pituitary, thyroid, ovary, breast, prostate, lung, esophagus, colon, and the central nervous system. It affects tumor invasiveness and recurrence in several systems, functions as a securin during cell cycle progression, and inhibits premature sister chromatid separation. PTTG is involved in multiple cellular pathways, including proliferation, DNA repair, transformation, angiogenesis induction, invasion, and the induction of genetic instability. In thyroid carcinomas, PTTG expression is a marker of invasiveness. PTTG is overexpressed in most pituitary adenomas, where it appears to correlate with recurrence and angiogenesis. Increasing evidence also points to the role of PTTG in endocrine organ development. For example, PTTG knockout mice show defective pancreatic b-cell proliferation. Herein, we review the current knowledge regarding PTTG-mediated pathways based on evidence from in vivo and in vitro studies as well as knockout mice models. We also summarize the issue of PTTG expression and its correlation with clinicopathologic parameters in patients with neoplasms, particularly of endocrine organs. In addition, we discuss in vitro and in vivo therapeutic models targeting PTTG overexpression.

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Inhibitory effect of acetyl-11-keto-β-boswellic acid on androgen receptor by interference of Sp1 binding activity in prostate cancer cells

Cited by 64 publications

References 27 publications

Targeting SP1 Transcription Factor in Prostate Cancer Therapy

Targeting SP1 Transcription Factor in Prostate Cancer Therapy

Pharmacological evidences for cytotoxic and antitumor properties of Boswellic acids from Boswellia serrata

Pituitary tumor-transforming gene in endocrine and other neoplasms: a review and update

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