Expression of the high mobility group A family member p8 is essential to maintaining tumorigenic potential by promoting cell cycle dysregulation in LβT2 cells

Brannon, Kate M.; Passe, Christina M. Million; White, Crystal; Bade, N. A.; King, Michael W.; Quirk, Christine C.

doi:10.1016/j.canlet.2007.03.011

Cited by 21 publications

(21 citation statements)

References 37 publications

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“…NUPR1 (also called p8 and com-1) is a small protein related to the high mobility group of transcriptional regulators. It is involved in different biological functions such as endoplasmic-reticulum stress response, programmed cell death, cell cycle progression and the control of gene expression by regulating chromatin accessibility [23]. Knockdown of NUPR1 expression in ETV5 overexpressing cells (HGE) resulted in a decrease migration capability compared with control cells.…”

Section: Discussionmentioning

confidence: 99%

Nidogen 1 and Nuclear Protein 1: novel targets of ETV5 transcription factor involved in endometrial cancer invasion

Pedrola

Devis

Llauradó

et al. 2015

Clin Exp Metastasis

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Endometrial cancer is the most frequent malignancy of the female genital tract in western countries. Our group has previously characterized the upregulation of the transcription factor ETV5 in endometrial cancer with a specific and significant increase in those tumor stages associated with myometrial invasion. We have shown that ETV5 overexpression in Hec1A endometrial cancer cells induces epithelial to mesenchymal transition resulting in the acquisition of migratory and invasive capabilities. In the present work, we have identified Nidogen 1 (NID1) and Nuclear Protein 1 (NUPR1) as direct transcriptional targets of ETV5 in endometrial cancer cells. Inhibition of NID1 and NUPR1 in ETV5 overexpressing cells reduced cell migration and invasion in vitro and reduced tumor growth and dissemination in an orthotopic endometrial cancer model. Importantly, we confirmed a significant increase of NUPR1 and NID1 protein expression in the invasion front of the tumor compared to their paired superficial zone, concomitant to ETV5 overexpression. Altogether, we conclude that NID1 and NUPR1 are novel targets of ETV5 and are actively cooperating with ETV5 at the invasion front of the tumor in the acquisition of an invasive phenotype to jointly drive endometrial cancer invasion.

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Section: Discussionmentioning

confidence: 99%

Nidogen 1 and Nuclear Protein 1: novel targets of ETV5 transcription factor involved in endometrial cancer invasion

Pedrola

Devis

Llauradó

et al. 2015

Clin Exp Metastasis

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“…NUPR1 was found to be a key gene involved in sensitizing serum-deprived astrocytes to oxidative stress via the p38 MAP kinase pathways [16]. The increase in NUPR1 mRNA was essential to the ability of several tissues to tolerate stress induced by systemic lipopolysaccharide (LPS) treatment, not as a mediator of tissue insult but rather an important part of the cellular stress manage- [23,24] f) Prostate cancer Expressed in lower levels in prostate cancer. NUPR1 levels inversely correlate with invasiveness and tumor progression.…”

Section: Nupr1 In Various Non-cancer Conditionsmentioning

confidence: 96%

“…NUPR1 underexpression caused defects in cell cycle checkpoints making the cells more prone to genetic instability and causing an increase in tumorigenic potential. NUPR1 was found to help the LβT2 cells avoid arrest at G 0 -G 1 which eventually caused the cells to accumulate more genetic defects [24].…”

Section: Nupr1 Potentiates Tumor Growth and Progressionmentioning

confidence: 99%

Emerging role of nuclear protein 1 (NUPR1) in cancer biology

Chowdhury

Samant

Fodstad

et al. 2009

Cancer Metastasis Rev

109

100

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NUPR1, or p8 or com1, was first identified from rat pancreas during acute pancreatitis and later as a gene whose expression was upregulated in metastatic breast cancer cells. NUPR1 is a molecule whose expression is upregulated in response to stress and is hence influenced by the host microenvironment. While NUPR1 has been implicated in several diseases, there is no singular biochemical pathway that can be attributed to its role in cancer. NUPR1 has been found to aid the establishment of metastasis and to play a key role in the progression of several malignancies including those of breast, thyroid, brain and pancreas. NUPR1 has been implicated in inducing chemoresistance in pancreatic and breast cancer cells, protecting them from apoptosis and making tumor cells genetically unstable. In prostate cancer, however, NUPR1 appears to have tumor suppressive activity. Understanding the mechanism of action of the multifaceted functions of NUPR1 may open up new dimensions towards creating novel therapies against cancer as well as other pathologies. This review draws on several published studies on NUPR1, mainly in cancer biology, and assesses NUPR1 from the perspective of its functional role in making cancer cells resistant to the action of conventional chemotherapeutic drugs.

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“…9 P8 participates in a wide range of biological functions in tumorigenesis, including anti-inflammatory, 10 cell cycle regulation, 11 autophagy, 12 and apoptosis inhibition. 13 Accumulating studies have shown that p8 is overexpressed in various cancer cells including pancreatic cancer, 14 colorectal carcinoma 15 and brain tumors.…”

Section: Introductionmentioning

confidence: 99%

p8 attenuates the apoptosis induced by dihydroartemisinin in cancer cells through promoting autophagy

Chen

Zeng

et al. 2015

Cancer Biology & Therapy

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Dihydroartemisinin (DHA) exhibits anticancer activities in a variety of cancer cells, but DHA alone are not effective enough for cancer therapy. In this study we found the stress-regulated protein p8 was obviously increased after DHA treatment in several cancer cells, which further to induce autophagy by the upregulation of endoplasmic reticulum stress-related protein ATF4 and CHOP. Furthermore, when we silenced p8 by siRNA in cancer cells, the apoptosis induced by DHA were notably increased, whereas the overexpression of p8 in cancer cells leaded to the resistance to DHA-induced apoptosis. Moreover, we found the inhibition of autophagy with chloroquine (CQ) can enhance the anticancer effect of DHA both in vitro and in vivo. In conclusion, we found that p8-mediated autophagy attenuates DHA-induced apoptosis in cancer cells, which provides evidence to support the use p8 as a cancer therapeutic target, and suggests that the combination treatment with DHA and autophagy inhibitor might be an effective cancer therapeutic strategy.

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Expression of the high mobility group A family member p8 is essential to maintaining tumorigenic potential by promoting cell cycle dysregulation in LβT2 cells

Cited by 21 publications

References 37 publications

Nidogen 1 and Nuclear Protein 1: novel targets of ETV5 transcription factor involved in endometrial cancer invasion

Nidogen 1 and Nuclear Protein 1: novel targets of ETV5 transcription factor involved in endometrial cancer invasion

Emerging role of nuclear protein 1 (NUPR1) in cancer biology

p8 attenuates the apoptosis induced by dihydroartemisinin in cancer cells through promoting autophagy

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