Microarray analysis reveals potential target genes of NF‐κB2/p52 in LNCaP prostate cancer cells

Nadiminty, Nagalakshmi; Dutt, Smitha S.; Tepper, Clifford G.; Gao, Allen C.

doi:10.1002/pros.21062

Cited by 33 publications

(28 citation statements)

References 43 publications

(53 reference statements)

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“…For example, Rnd3 induction has been linked to the transcription factor NFkB in prostate cancer cells [15]. In addition, the oncogene B-Raf induces its expression in melanoma cells [16,17].…”

Section: Rnd Expression Is Regulated By Diverse Stimuli Transcriptionmentioning

confidence: 99%

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

2010

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Rnd3/RhoE has two distinct functions, regulating the actin cytoskeleton and cell proliferation. This might explain why its expression is often altered in cancer and by multiple stimuli during development and disease. Rnd3 together with its relatives Rnd1 and Rnd2 are atypical members of the Rho GTPase family in that they do not hydrolyse GTP. Rnd3 and Rnd1 both antagonise RhoA/ROCK-mediated actomyosin contractility, thereby regulating cell migration, smooth muscle contractility and neurite extension. In addition, Rnd3 has been shown to have a separate role in inhibiting cell cycle progression by reducing translation of cell cycle regulators, including cyclin D1 and Myc. We propose that Rnd3 could act as a tumour suppressor to limit proliferation, but when mutations bypass this activity of Rnd3, it can promote cancer invasion through its effects in the actin cytoskeleton.

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Section: Rnd Expression Is Regulated By Diverse Stimuli Transcriptionmentioning

confidence: 99%

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

2010

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“…32 For this purpose, we determined CXCl-1 and CXCL-10 transcript levels in A549 lung cancer cells treated with Nutlin-3 or vehicle (DMSO), by QPCR. The data (Fig.…”

Section: Mdm2 Elevates Expression Of Nf-κb2 Target Gene Cxcl-1 or 10mentioning

confidence: 99%

Human Oncoprotein MDM2 Up-regulates Expression of NF- B2 Precursor p100 Conferring a Survival Advantage to Lung Cells

Vaughan

Mohanraj

Singh³

et al. 2011

Genes & Cancer

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The current model predicts that MDM2 is primarily overexpressed in cancers with wild-type (WT) p53 and contributes to oncogenesis by degrading p53. Following a correlated expression of MDM2 and NF-κB2 transcripts in human lung tumors, we have identified a novel transactivation function of MDM2. Here, we report that in human lung tumors, overexpression of MDM2 was found in approximately 30% of cases irrespective of their p53 status, and expression of MDM2 and NF-κB2 transcripts showed a highly significant statistical correlation in tumors with WT p53. We investigated the significance of this correlated expression in terms of mechanism and biological function. Increase in MDM2 expression from its own promoter in transgenic mice remarkably enhanced expression of NF-κB2 compared with its non-transgenic littermates. Knockdown or elimination of endogenous MDM2 expression in cultured non-transformed or lung tumor cells drastically reduced expression of NF-κB2 transcripts, suggesting a normal physiological role of MDM2 in regulating NF-κB2 transcription. MDM2 could up-regulate expression of NF-κB2 transcripts when its p53-interaction domain was blocked with Nutlin-3, indicating that the MDM2-p53 interaction is dispensable for up-regulation of NF-κB2 expression. Consistently, analysis of functional domains of MDM2 indicated that although the p53-interaction domain of MDM2 contributes to the up-regulation of the NFκB2 promoter, MDM2 does not require direct interactions with p53 for this function. Accordingly, MDM2 overexpression in non-transformed or lung cancer cells devoid of p53 also generated a significant increase in the expression of NF-κB2 transcript and its targets CXCL-1 and CXCL-10, whereas elimination of MDM2 expression had the opposite effects. MDM2-mediated increase in p100/NF-κB2 expression reduced cell death mediated by paclitaxel. Furthermore, knockdown of NF-κB2 expression retarded cell proliferation. Based on these data, we propose that MDM2-mediated NF-κB2 up-regulation is a combined effect of p53-dependent and independent mechanisms and that it confers a survival advantage to lung cancer cells.

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“…qRT-PCR analyses were performed as described previously (19,20). (Sequences of primers are listed in the supplemental methods.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA let-7c Suppresses Androgen Receptor Expression and Activity via Regulation of Myc Expression in Prostate Cancer Cells

Nadiminty

Tummala

Lou

et al. 2012

Journal of Biological Chemistry

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168

140

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Background: Let-7c is a microRNA down-regulated in prostate cancer. Results: Let-7c suppresses androgen receptor expression by targeting its transcription via c-Myc. Suppression of AR by let-7c leads to decreased cell proliferation and tumor growth. Conclusion: Let-7c suppresses androgen receptor expression. Significance: Our study demonstrates that let-7c plays an important role in regulation of androgen signaling and prostate cancer proliferation.

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Microarray analysis reveals potential target genes of NF‐κB2/p52 in LNCaP prostate cancer cells

Abstract: This study provides a comprehensive analysis of genes potentially regulated by NF-kappaB2/p52 in the LNCaP prostate cancer cell line and provides a rationale for the induction of castration-resistant growth by p52 in LNCaP cells.

Cited by 33 publications

References 43 publications

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

Human Oncoprotein MDM2 Up-regulates Expression of NF- B2 Precursor p100 Conferring a Survival Advantage to Lung Cells

MicroRNA let-7c Suppresses Androgen Receptor Expression and Activity via Regulation of Myc Expression in Prostate Cancer Cells

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