Cooperation of loss of <i>NKX3.1</i> and inflammation in prostate cancer initiation

Magnen, Clémentine Le; Virk, Renu K.; Dutta, Amitabh; Kim, Jaime Yeji; Panja, Sukanya; Lopez‐Bujanda, Zoila A.; Califano, Andrea; Drake, Charles G.; Mitrofanova, Antonina; Abate‐Shen, Cory

doi:10.1242/dmm.035139

Cited by 35 publications

(26 citation statements)

References 45 publications

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“…Second, prostatitis is known to increase the risk of PCa [38] and alcohol enhances inflammation. Furthermore, chronic inflammation is known to create an immunosuppressive environment that negate antitumor immunity [39,40]. This provides an advantage for tumor formation and progression [41].…”

Section: Discussionmentioning

confidence: 99%

Alcohol Consumption and the Risk of Prostate Cancer: A Dose-Response Meta-Analysis

et al. 2020

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Alcohol is widely consumed and is known as a major risk factor for several types of cancers. Yet, it is unclear whether alcohol consumption is associated with the risk of prostate cancer (PCa) or not. We conducted linear and non-linear dose–response meta-analyses of cohort studies on alcohol consumption and PCa risk by types of alcohol (total, wine, beer, and liquor) and PCa (non-aggressive and aggressive). Pubmed and Embase were searched through April 2020 to identify relevant studies. Summary relative risk (RR) and 95% confidence interval (CI) were estimated using a random-effects model. For non-aggressive PCa, by alcohol type, the risk increased linearly with liquor (RR per 14 g/day intake (alcohol content in standard drink) being 1.04 (95% CI = 1.02–1.06, I2 = 0%, three studies) and non-linearly with beer (Pnon-linearity = 0.045, four studies), with increased risk observed in the lower range (RR = 1.03, 95% CI = 1.01–1.05; 14 g/day), with 1.05 (95% CI = 1.01–1.08) at 28 g/day. Wine was not significantly associated with the risk of non-aggressive PCa. For aggressive PCa, a non-linear relationship of diverse shapes was indicated for all types of alcohol in the sensitivity analysis. Compared to non-drinking, a significant positive association was more apparent at lower dose for liquor (RR = 1.12, 95% CI = 1.04–1.20 at 14 g/day; RR = 1.16, 95% CI = 1.03–1.31 at 28 g/day; Pnon-linearity = 0.005, three studies) but at higher doses for wine (RR = 1.02, 95% CI = 0.90–1.16 at 28 g/day, RR = 1.35, 95% CI = 1.08–1.67 at 56 g/day; Pnon-linearity = 0.01, four studies). In contrast, decreased risks were indicated at lower doses of beer (RR = 0.85, 95% CI = 0.79–0.92 at 14 g/day; RR = 0.79, 95% CI = 0.70–0.90 at 28 g/day, Pnon-linearity < 0.001, four studies). Total alcohol consumption was not associated with both types of PCa. In this study, we found heterogeneous associations between alcohol intake and PCa by types of alcohol and PCa.

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Section: Discussionmentioning

confidence: 99%

Alcohol Consumption and the Risk of Prostate Cancer: A Dose-Response Meta-Analysis

et al. 2020

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“…Lineage plasticity, the ability of committed cells to change cell states through dedifferentiation or transdifferentiation, is an important mechanism for tissue repair ( Ge and Fuchs, 2018 ; Rajagopal and Stanger, 2016 ; Wahl and Spike, 2017 ). Cancer can co-opt this normal repair program to promote its initiation and progression ( Ge and Fuchs, 2018 ; Le Magnen et al, 2018 ). Un-like normal tissues, where lineage plasticity is a transient state during tissue repair, cancer cells exhibit persistent plasticity.…”

Section: Introductionmentioning

confidence: 99%

Stem Cell Determinant SOX9 Promotes Lineage Plasticity and Progression in Basal-like Breast Cancer

et al. 2020

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SUMMARY Lineage plasticity is important for the development of basal-like breast cancer (BLBC), an aggressive cancer subtype. While BLBC is likely to originate from luminal progenitor cells, it acquires substantial basal cell features and contains a heterogenous collection of cells exhibiting basal, luminal, and hybrid phenotypes. Why luminal progenitors are prone to BLBC transformation and what drives luminal-to-basal reprogramming remain unclear. Here, we show that the transcription factor SOX9 acts as a determinant for estrogen-receptor-negative (ER − ) luminal stem/progenitor cells (LSPCs). SOX9 controls LSPC activity in part by activating both canonical and non-canonical nuclear factor κB (NF-κB) signaling. Inactivation of TP53 and RB via expression of SV40 TAg in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-basal reprogramming in vivo . Furthermore, SOX9 deletion inhibits the progression of ductal carcinoma in situ (DCIS)-like lesions to invasive carcinoma. These data show that ER − LSPC determinant SOX9 acts as a lineage plasticity driver for BLBC progression.

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“…Schematic demonstration of changes in the expression profile of homeobox family genes in the control and ERN1 knockdown glioma cells under glucose deprivation; NS -no significant changes. with suppression of ERN1 knockdown glioma cells proliferation (Auf et al 2010) because this transcription factor functions as a tumor suppressor and can inhibits proliferation as well as invasion (Le Magnen et al 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Transcription factors play an important role in the malignant tumor growth, preferentially through ERN1 (endoplasmic reticulum to nucleus signaling 1) signaling pathway of endoplasmic reticulum stress (Minchenko et al 2015b, c;Tsymbal et al 2016a). The homeobox proteins represent an important group of transcription factors, which are related to tumorigenesis and has been largely investigated (Kataoka et al 2001;Guca et al 2018;Le Magnen et al 2018;Miyashita et al 2018;Chen et al 2019;Hamaidi et al 2019;Li et al 2019;Wang et al 2019). Recently, it was shown that transcriptional inhibitor ZEB2 (zinc finger E-box binding homeobox 2) functions as oncogene in human laryngeal squamous cell carcinoma (Li et al 2019).…”

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confidence: 99%

“…Homeobox-containing transcription factor NKX3-1 (NKX3A or NK3 homeobox 1) functions as a negative regulator of epithelial cell growth in prostate tissue and its aberrant expression is associated with prostate tumor progression as a tumor suppressor, because it can inhibit proliferation and invasion activities of PC-3 prostate cancer cells (Le Magnen et al 2018). Furthermore, NKX3-1 is required for induced pluripotent stem cell reprogramming and can replace OCT4 and generate fully pluripotent stem cells (Mai et al 2018).…”

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confidence: 99%

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ERN1 knockdown modifies the effect of glucose deprivation on homeobox gene expressions in U87 glioma cells

Tsymbal

Minchenko

Khita

et al. 2020

Endocrine Regulations

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Objective. The aim of the present investigation was to study the expression of genes encoding homeobox proteins ZEB2 (zinc finger E-box binding homeobox 2), TGIF1 (TGFB induced factor homeobox 1), SPAG4 (sperm associated antigen 4), LHX1 (LIM homeobox 1), LHX2, LHX6, NKX3-1 (NK3 homeobox 1), and PRRX1 (paired related homeobox 1) in U87 glioma cells in response to glucose deprivation in control glioma cells and cells with knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1), the major pathway of the endoplasmic reticulum stress signaling, for evaluation of it possible significance in the control of glioma growth through ERN1 signaling and chemoresistance.Methods. The expression level of homeobox family genes was studied in control (transfected by vector) and ERN1 knockdown U87 glioma cells under glucose deprivation condition by real-time quantitative polymerase chain reaction.Results. It was shown that the expression level of ZEB2, TGIF1, PRRX1, and LHX6 genes was up-regulated in control glioma cells treated by glucose deprivation. At the same time, the expression level of three other genes (NKX3-1, LHX1, and LHX2) was down-regulated. Furthermore, ERN1 knockdown of glioma cells significantly modified the effect glucose deprivation condition on the expression almost all studied genes. Thus, treatment of glioma cells without ERN1 enzymatic activity by glucose deprivation condition lead to down-regulation of the expression level of ZEB2 and SPAG4 as well as to more significant up-regulation of PRRX1 and TGIF1 genes. Moreover, the expression of LHX6 and NKX3-1 genes lost their sensitivity to glucose deprivation but LHX1 and LHX2 genes did not change it significantly.Conclusions. The results of this investigation demonstrate that ERN1 knockdown significantly modifies the sensitivity of most studied homeobox gene expressions to glucose deprivation condition and that these changes are a result of complex interaction of variable endoplasmic reticulum stress related and unrelated regulatory factors and contributed to glioma cell growth and possibly to their chemoresistance.

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Cooperation of loss of NKX3.1 and inflammation in prostate cancer initiation

Cited by 35 publications

References 45 publications

Alcohol Consumption and the Risk of Prostate Cancer: A Dose-Response Meta-Analysis

Alcohol Consumption and the Risk of Prostate Cancer: A Dose-Response Meta-Analysis

Stem Cell Determinant SOX9 Promotes Lineage Plasticity and Progression in Basal-like Breast Cancer

ERN1 knockdown modifies the effect of glucose deprivation on homeobox gene expressions in U87 glioma cells

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