Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells

Tano, Keiko; Onoguchi‐Mizutani, Rena; Yeasmin, Fouzia; Uchiumi, Fumiaki; Suzuki, Yutaka; Yada, Tetsushi; Akimitsu, Nobuyoshi

doi:10.3389/fgene.2017.00208

Cited by 28 publications

(23 citation statements)

References 25 publications

(36 reference statements)

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“…27 Silencing of MALAT1 suppresses the activation of several factors including JNK1, overexpressed MALAT1 results in their phosphorylation, 28 and MALAT1 could regulate or influence the activity and expression of p53 in disease related to lung. 29,30 Additionally, MALAT1 overexpression suppressed cell apoptosis in bronchopulmonary dysplasia. The extracellular ROS of neutrophils in each group.…”

Section: Discussionmentioning

confidence: 98%

Silencing of lncRNA MALAT1 Prevents Inflammatory Injury after Lung Transplant Ischemia-Reperfusion by Downregulation of IL-8 via p300

Han

et al. 2019

Molecular Therapy - Nucleic Acids

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Ischemia-reperfusion injury is a common early complication after lung transplantation. It was reported that long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in ischemia-reperfusion injury and regulates inflammation. This study aimed to explore the role of MALAT1 in inflammatory injury following lung transplant ischemia-reperfusion (LTIR). A LTIR rat model was successfully established, with the expression of MALAT1 and interleukin-8 (IL-8) in lung tissues detected. Then, in vitro loss- and gain-of-function investigations were conducted to evaluate the effect of MALAT1 on pulmonary epithelial cell apoptosis and IL-8 expression. The relationship among MALAT1, p300, and IL-8 was tested. Moreover, a sh-MALAT1-mediated model of LTIR was established in vivo to examine inflammatory injury and chemotaxis infiltration. Both IL-8 and MALAT1 were highly expressed in LTIR. MALAT1 interacted with p300 to regulate the IL-8 expression by recruiting p300. Importantly, silencing of MALAT1 inhibited the chemotaxis of neutrophils by downregulating IL-8 expression via binding to p300. Besides, MALAT1 silencing alleviated the inflammatory injury after LTIR by downregulating IL-8 and inhibiting infiltration and activation of neutrophils. Collectively, these results demonstrated that silencing of MALAT1 ameliorated the inflammatory injury after LTIR by inhibiting chemotaxis of neutrophils through p300-mediated downregulation of IL-8, providing clinical insight for LTIR injury.

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Section: Discussionmentioning

confidence: 98%

Silencing of lncRNA MALAT1 Prevents Inflammatory Injury after Lung Transplant Ischemia-Reperfusion by Downregulation of IL-8 via p300

Han

et al. 2019

Molecular Therapy - Nucleic Acids

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“…In light of the above, much more research into phase separation in cancer progression is required to gain medical benefits from therapeutic strategies, early and accurate diagnosis and cancer prevention. 310,311]; DNA repair foci [34]; gem, Gemini of Cajal body [312,313], histone locus body, [310]; keratin granule [314]; nuclear pore complex [315,316]; nuclear speckle [7, [317][318][319][320][321][322]; nucleolus [323][324][325][326]; virus factory [327][328][329][330];…”

Section: Accepted Articlementioning

confidence: 99%

Aberrant phase separation and cancer

Taniue

Akimitsu

2021

The FEBS Journal

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Eukaryotic cells are intracellularly divided into numerous compartments or organelles, which coordinate specific molecules and biological reactions. Membrane-bound organelles are physically separated by lipid bilayers from the surrounding environment. Biomolecular condensates, also referred to membraneless organelles, are micron-scale cellular compartments that lack membranous enclosures but function to concentrate proteins and RNA molecules, and these are involved in diverse processes. Liquid-liquid phase separation (LLPS) driven by multivalent weak macromolecular interactions is a critical principle for the formation of biomolecular condensates, and a multitude of combinations among multivalent interactions may drive liquid-liquid phase transition (LLPT). Dysregulation of LLPS and LLPT leads to aberrant condensate and amyloid formation, which causes many human diseases, including neurodegeneration and cancer. Here, we describe recent findings regarding abnormal forms of biomolecular condensates and aggregation via aberrant LLPS and LLPT of cancer-related proteins in cancer development driven by mutation and fusion of genes. Moreover, we discuss the regulatory mechanisms by which aberrant LLPS and LLPT occur in cancer and the drug candidates targeting these mechanisms. Further understanding of the molecular events regulating how biomolecular condensates and aggregation form in cancer tissue is critical for the development of therapeutic strategies against tumorigenesis.

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“…MALAT1 binds with serine/arginine splicing factor (SR) in the nuclear speckle domains and increases SR phosphorylation followed by regulation of the alternative splicing of pre-mRNA (42). MALAT1 suppresses p53 activity by binding to a minimal region of p53 promoter that regulates downstream genes influencing the cell cycle progression of lung cancer cells (43). Downregulation of MALAT1 has been shown to inhibit NSCLC progression by inhibiting autophagy (44).…”

Section: Biologic Functions and Molecular Mechanisms Of Ln- Crnas mentioning

confidence: 99%

Long non‑coding RNAs in lung cancer: Regulation patterns, biologic function and diagnosis implications (Review)

Jiang

Wang

2019

Int J Oncol

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Lung cancer is the most common malignancy with the highest mortality worldwide. Emerging research has demonstrated that long non-coding RNAs (lncRNAs), a key genomic product, are commonly dysregulated in lung cancer and have significant functions in lung cancer initiation, progression and therapeutic response. lncRNAs may interact with DNA, RNA or proteins, as tumor suppressor genes or oncogenes, to regulate gene expression and cell signaling pathways. In the present review, first a summary was presented of the causal effects of dysregulated lncRNAs in lung cancer. Next, the function and specific mechanisms of lncRNA-mediated tumorigenesis, metastasis and drug resistance in lung cancer were discussed. Finally, the potential roles of lncRNAs as biomarkers for lung cancer were explored.

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Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells

Cited by 28 publications

References 25 publications

Silencing of lncRNA MALAT1 Prevents Inflammatory Injury after Lung Transplant Ischemia-Reperfusion by Downregulation of IL-8 via p300

Silencing of lncRNA MALAT1 Prevents Inflammatory Injury after Lung Transplant Ischemia-Reperfusion by Downregulation of IL-8 via p300

Aberrant phase separation and cancer

Long non‑coding RNAs in lung cancer: Regulation patterns, biologic function and diagnosis implications (Review)

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