NOK mediates glycolysis and nuclear PDC associated histone acetylation

Shi, Weiye; Yang, Xiao; Huang, Bo; Shen, Wen Hong; Liu, Li

doi:10.2741/4572

Cited by 30 publications

(14 citation statements)

References 20 publications

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“…In addition to these coding transcripts, the long noncoding transcript metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was expressed in all cells from all patients. MALAT1 acts as a transcriptional regulator controlling expression of a number of genes involved in metastasis and prognosis in a variety of cancers [ 56 , 57 ], including lung cancer [ 58 ] and in PDAC [ 59 ]. In fact, in terms of expression levels, MALAT1 and CD74 were the 6 th & 7 th most highly expressed transcripts (for reference, mitochondrial 16S rRNA was the most highly expressed transcript, followed by 4 other mitochondrial genes).…”

Section: Resultsmentioning

confidence: 99%

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

et al. 2017

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Here we describe isolation and characterization of macrophage-tumor cell fusions (MTFs) from the blood of pancreatic ductal adenocarcinoma (PDAC) patients. The MTFs were generally aneuploidy, and immunophenotypic characterizations showed that the MTFs express markers characteristic of PDAC and stem cells, as well as M2-polarized macrophages. Single cell RNASeq analyses showed that the MTFs express many transcripts implicated in cancer progression, LINE1 retrotransposons, and very high levels of several long non-coding transcripts involved in metastasis (such as MALAT1). When cultured MTFs were transplanted orthotopically into mouse pancreas, they grew as obvious well-differentiated islands of cells, but they also disseminated widely throughout multiple tissues in “stealth” fashion. They were found distributed throughout multiple organs at 4, 8, or 12 weeks after transplantation (including liver, spleen, lung), occurring as single cells or small groups of cells, without formation of obvious tumors or any apparent progression over the 4 to 12 week period. We suggest that MTFs form continually during PDAC development, and that they disseminate early in cancer progression, forming “niches” at distant sites for subsequent colonization by metastasis-initiating cells.

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Section: Resultsmentioning

confidence: 99%

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

et al. 2017

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“…MALAT1 expression has been shown to be either upregulated or downregulated in human cancers. On one hand, upregulation of MALAT1 was reported in lung cancer, hepatocellular carcinoma, breast cancer, and colorectal carcinoma, which has been extensively reviewed previously [23,24,25,26]. On the other hand, several studies showed that the expression of MALAT1 is downregulated in glioma [27], colorectal cancer [28], and breast cancer [29,30].…”

Section: Is Malat1 a Metastasis Promoter Or A Metastasis Suppressor?mentioning

confidence: 99%

New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis

Sun

2019

Cancers

246

171

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However, Malat1 knockout mice develop and grow normally, and do not show alterations in alternative splicing. While MALAT1 was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for MALAT1 is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating MALAT1 have been observed, which led to distinct models for MALAT1′s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study MALAT1′s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.

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“… 6 , 7 As one of the most abundant LncRNAs, MALAT1 is differentially expressed in various cancers, 8 , 9 with complex and extensive functions during the development and progression of the cancers. 10 Highly expressed in prostate cancer tissues and cell lines, it promotes the cells to proliferate and invade and inhibits their apoptosis in patients with prostate cancer. 11 In a study by Chen et al, the increasing expression of serum MALAT1 shortens the survival time of patients with EOC, so MALAT1 can be used as a biomarker for diagnosing metastasis.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA MALAT1 Promotes Survival of Epithelial Ovarian Cancer Cells by Downregulating miR-145-5p</p>

Wang

Zhao

Wang

2020

CMAR

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This paper was aimed at investigating the regulatory mechanism of long noncoding RNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) in epithelial ovarian cancer (EOC). Materials and Methods: MALAT1 and miR-145-5p expression in the tissues, serum, and EOC cell lines (TOV-112D, TOV-21G) of patients with EOC were detected. The two genes were transfected into the cells via upregulating or downregulating their expression. Levels of apoptosis-related proteins (Caspase-3, Bax, Bcl-2) were analyzed. Mechanisms of cell proliferation, invasion, and apoptosis were studied. Results: MALAT1 was high expressed in EOC tissues, while miR-145-5p was poorly expressed in them. The areas under the curves (AUCs) of the two genes for diagnosing EOC were greater than 0.850, and the two had a significantly negative correlation. According to multivariate Cox regression analysis, high MALAT1 expression, tumor size, degree of differentiation, case staging, and lymph node metastasis were the independent risk factors affecting prognosis. The 5-year overall survival rate (OSR) of patients with low MALAT1 expression was remarkably higher than that of those with high expression. Overexpressing miR-145-5p and silencing MALAT1 could inhibit EOC cells from proliferating and invading, increase their apoptotic rate, and improve levels of the apoptosis-related proteins. After cotransfection with MALAT1-inhibitor + miR-145-5p-inhibitor, the proliferation and invasion of TOV-112D and TOV-21G cells were inhibited and the apoptotic rate rose more obviously. Inhibiting MALAT1 could increase miR-145-5p expression, thus inhibiting EOC cells from proliferating and invading and thereby increasing their apoptotic rate. Conclusion: MALAT1 promotes EOC cells' survival by downregulating miR-145-5p so it may become a new direction for EOC diagnosis and gene therapy.

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NOK mediates glycolysis and nuclear PDC associated histone acetylation

Cited by 30 publications

References 20 publications

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

"Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma

New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis

<p>LncRNA MALAT1 Promotes Survival of Epithelial Ovarian Cancer Cells by Downregulating miR-145-5p</p>

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