Correlation of low expression of hMOF with clinicopathological features of colorectal carcinoma, gastric cancer and renal cell carcinoma

Cao, Lingling; Zhu, Lin; Yang, Jiaxing; Su, Jiaming; Ni, Jinsong; Du, Yujun; Liu, Da; Wang, Yanfang; Wang, Fei; Jin, Jingji; Cai, Yong

doi:10.3892/ijo.2014.2266

Cited by 57 publications

(47 citation statements)

References 34 publications

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“…H4K16ac and MOF are known to be associated with tumorigenesis and heterogeneity [32,33]. We report for the first time that low-level MOF-induced downregulation of H4K16ac is a downstream target of Notch signaling in human HCC and breast cancer.…”

Section: Discussionmentioning

confidence: 82%

MDM2–MOF–H4K16ac axis contributes to tumorigenesis induced by Notch

et al. 2014

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Identification of the epigenetic mechanisms involved in the transmission of Notch signaling is useful for personalized medicine. We observed that aberrantly high levels of Notch activity resulted in H4K16ac downregulation in hepatocellular carcinoma and breast cancer cell lines and tissues. This downregulated acetylation was a consequence of increased male on the first degradation following the upregulation of full‐length murine double minute 2 in different cancer types. We observed that increases in male on the first could attenuate heterogeneity induced by aberrantly high levels of Notch activity. Our results provide new insights into the analysis and treatment of Notch‐induced hepatocellular carcinoma and breast cancer.

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Section: Discussionmentioning

confidence: 82%

MDM2–MOF–H4K16ac axis contributes to tumorigenesis induced by Notch

et al. 2014

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“…MOF plays important roles in transcription activation, DNA damage response, and maintenance of embryonic stem cell pluripotency (Gupta et al, 2005(Gupta et al, , 2014Li et al, 2010Li et al, , 2012Sharma et al, 2010). Compared with normal tissues, expression of MOF is frequently downregulated in several types of solid tumors (Cao et al, 2014;Liu et al, 2013;Pfister et al, 2008;Zhang et al, 2014). However, there are also reports that MOF expression is elevated in certain cancers and MOF may stimulate cell proliferation and transformation (Gupta et al, 2008;Zhao et al, 2013a).…”

Section: Introductionmentioning

confidence: 95%

MOF Acetylates the Histone Demethylase LSD1 to Suppress Epithelial-to-Mesenchymal Transition

Luo

Shenoy

et al. 2016

Cell Reports

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The histone demethylase LSD1 facilitates epithelial-to-mesenchymal transition (EMT) and tumor progression by repressing epithelial marker expression. However, little is known about how its function may be modulated. Here, we report that LSD1 is acetylated in epithelial but not mesenchymal cells. Acetylation of LSD1 reduces its association with nucleosomes, thus increasing histone H3K4 methylation at its target genes and activating transcription. The MOF acetyltransferase interacts with LSD1 and is responsible for its acetylation. MOF is preferentially expressed in epithelial cells and is downregulated by EMT-inducing signals. Expression of exogenous MOF impedes LSD1 binding to epithelial gene promoters and histone demethylation, thereby suppressing EMT and tumor invasion. Conversely, MOF depletion enhances EMT and tumor metastasis. In human cancer, high MOF expression correlates with epithelial markers and a favorable prognosis. These findings provide insight into the regulation of LSD1 and EMT and identify MOF as a critical suppressor of EMT and tumor progression.

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“…In recent years, the effects of hMOF on the occurrence and development of malignant tumors has been a hot area of study in international academia. Previous studies indicated that hMOF is frequently downregulated in primary breast carcinoma and medulloblastoma (19), human renal cell (20), and colorectal carcinoma, and gastric cancer (23). However, the expression of hMOF was reportedly much higher in NSCLC compared to corresponding normal tissues, and hMOF promoted the proliferation, metastasis and adhesion of NSCLC cell lines (21).…”

Section: Discussionmentioning

confidence: 98%

Expression of hMOF in different ovarian tissues and its effects on ovarian cancer prognosis

Cai

Liu

et al. 2014

Oncology Reports

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Abstract. Human MOF (hMOF) is a major acetylase of human H4K16 involved in the regulation of physiological and pathological processes. We investigated the expression of hMOF in different ovarian tissues and its correlation with ovarian cancer prognosis. Reverse transcription PCR and western blot analysis were used to detect hMOF mRNA and protein expression, respectively, in different ovarian tissues. Immunohistochemistry was also performed to detect hMOF expression in different ovarian tissues, including ovarian epithelial cancer, borderline tumor, benign tumor and normal ovarian tissues. In addition, the relationships between hMOF expression and clinicopathological ovarian cancer data were analyzed. The Cox proportional-hazards regression model was used to analyze the factors associated with ovarian cancer prognosis. To analyze the effects of hMOF expression on ovarian cancer prognosis, a survival curve was plotted from the follow-up data of 77 patients with ovarian cancer. Compared with normal ovarian tissues, hMOF mRNA and protein expression was significantly decreased in ovarian epithelial cancer tissues. The proportions of high hMOF expression in normal and benign ovarian epithelial tumor tissues, were much higher than those in ovarian epithelial cancer tissues. Furthermore, hMOF protein expression was closely associated with the ovarian cancer stage. The expression of hMOF protein was determined as an independent risk factor influencing ovarian cancer prognosis. Patients with high hMOF levels showed improved survival than those with low hMOF levels. hMOF mRNA and protein expression decreased in ovarian epithelial cancer, thus the hMOF protein potentially serves as a new clinical marker of ovarian cancer prognosis.

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Correlation of low expression of hMOF with clinicopathological features of colorectal carcinoma, gastric cancer and renal cell carcinoma

Cited by 57 publications

References 34 publications

MDM2–MOF–H4K16ac axis contributes to tumorigenesis induced by Notch

MDM2–MOF–H4K16ac axis contributes to tumorigenesis induced by Notch

MOF Acetylates the Histone Demethylase LSD1 to Suppress Epithelial-to-Mesenchymal Transition

Expression of hMOF in different ovarian tissues and its effects on ovarian cancer prognosis

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