The lncRNA HOTAIR transcription is controlled by HNF4α-induced chromatin topology modulation

Battistelli, Cecilia; Sabarese, Giovanna; Santangelo, Laura; Montaldo, Claudia; Gonzalez, Frank J.; Tripodi, Marco; Cicchini, Carla

doi:10.1038/s41418-018-0170-z

Cited by 64 publications

(51 citation statements)

References 45 publications

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“…This suggested that repression of HOTAIR could be clinically helpful to suppress oesophageal cancer progression and HOTAIR could be a promising target for oesophageal cancer treatment. However, an additional molecular mechanism by which HOTAIR works has been reported involving mediation on epithelial genes expression (ie E‐cadherin) through the recruitment of PRC2 . Therefore, more researches on mechanisms of HOTAIR‐based oesophageal cancer therapeutics are required to explore the application potential.…”

Section: Discussionmentioning

confidence: 99%

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Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

Wang

Tan²,

Zhuang³

et al. 2019

J Cellular Molecular Medi

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Oesophageal cancer is a progressive tumour with high mortality. However, therapies aimed at treating oesophageal cancer remain relatively limited. Accumulating studies have highlighted long non‐coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), microRNA‐204 (miR‐204) and homeobox C8 (HOXC8) in the progression of oesophageal cancer. Herein, we tried to demonstrate the function of HOTAIR, miR‐204 and HOXC8 in oesophageal cancer and their relationship. Differentially expressed genes involved in oesophageal cancer were identified. The endogenous expression of HOTAIR and miR‐204 in oesophageal cancer cell lines was altered to elucidate their effects and to identify the interaction among HOTAIR, miR‐204 and HOXC8. We also explored the underlying regulatory mechanisms of HOTAIR and miR‐204 with siRNA against HOTAIR, miR‐204 mimic or miR‐204 inhibitor. Cell proliferation, migration, invasion and apoptosis were subsequently detected. Xenograft in nude mice was induced to evaluate tumourigenicity. miR‐204 was down‐regulated, while HOTAIR and HOXC8 were up‐regulated in the oesophageal cancer tissues. HOTAIR could competitively bind to miR‐204 and miR‐204 could further target HOXC8. The oesophageal cancer cells treated with si‐HOTAIR or miR‐204 mimic exhibited decreased expression levels of HOXC8, Vimentin and MMP‐9, but increased E‐cadherin level. Silenced HOTAIR or elevated miR‐204 inhibited proliferation, migration and invasion, along with stimulated apoptosis of oesophageal cancer cells. In summary, our results show that lncRNA HOTAIR could specifically bind to miR‐204 as a competing endogenous RNA and regulate miR‐204 and HOXC8. Hence, down‐regulation of HOTAIR could inhibit progression of oesophageal cancer, indicating a novel target for oesophageal cancer treatment.

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Section: Discussionmentioning

confidence: 99%

“…However, an additional molecular mechanism by which HOTAIR works has been reported involving mediation on epithelial genes expression (ie E-cadherin) through the recruitment of PRC2. 49,50 Therefore, more researches on mechanisms of HOTAIR-based oesophageal cancer therapeutics are required to explore the application potential.…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

Wang

Tan²,

Zhuang³

et al. 2019

J Cellular Molecular Medi

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“…While HNF4A has mainly been described as a transcriptional activator promoting recruitment of coactivators [ 43 , 44 , 45 , 46 ], reports have also indicated that HNF4A interacted with corepressors [ 47 , 48 ] and may have acted as a direct repressor in some instances [ 26 , 49 ]. This is in line with the context-specific activities of TFs and cofactors, which are increasingly recognized as versatile transcriptional regulators with the potential to both positively or negatively impact on gene expression [ 50 ].…”

Section: Hnf4 Is a Cell-type Specific Tf Required For Cell Identitmentioning

confidence: 99%

Control of Cell Identity by the Nuclear Receptor HNF4 in Organ Pathophysiology

Dubois

Staels

Lefèbvre

et al. 2020

Cells

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Hepatocyte Nuclear Factor 4 (HNF4) is a transcription factor (TF) belonging to the nuclear receptor family whose expression and activities are restricted to a limited number of organs including the liver and gastrointestinal tract. In this review, we present robust evidence pointing to HNF4 as a master regulator of cellular differentiation during development and a safekeeper of acquired cell identity in adult organs. Importantly, we discuss that transient loss of HNF4 may represent a protective mechanism upon acute organ injury, while prolonged impairment of HNF4 activities could contribute to organ dysfunction. In this context, we describe in detail mechanisms involved in the pathophysiological control of cell identity by HNF4, including how HNF4 works as part of cell-specific TF networks and how its expression/activities are disrupted in injured organs.

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“…Cells were seeded at the density of 5,000 cells per well in 96-well plates (Bagati et al, 2018). After treatment, cells were added in 20 µl of the 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyl tetrazolium bromide (MTT) reagent (Solarbio) and incubated for 4 hr (Battistelli et al, 2019;Fan et al, 2018). After medium removal, 200 µl dimethyl sulfoxide (Sigma-Aldrich) was added to dissolve the blue formazan, and the absorbance of the solution was measured at 570 nm (Cheignon et al, 2018).…”

Section: Cell Viability Assaymentioning

confidence: 99%

MKP1 reduces neuroinflammation via inhibiting endoplasmic reticulum stress and mitochondrial dysfunction

Huang

Jiang

2019

Journal Cellular Physiology

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MAP kinase phosphatase 1 (MKP1) has been identified as an antiapoptotic protein via sustaining mitochondrial function. However, the role of MKP1 in neuroinflammation has not been fully understood. The aim of this study is to figure out the influence of MKP1 in lipopolysaccharide (LPS)-treated microglia BV-2 cells and investigate whether MKP1 reduces BV-2 cell death via modulating endoplasmic reticulum (ER) stress and mitochondrial dysfunction. The results of this study demonstrated that MKP1 was rapidly downregulated after exposure to LPS. However, the transfection of MKP1 adenovirus could reverse cell viability and attenuate LPS-mediated BV-2 cell apoptosis. Mechanistically, MKP1 overexpression alleviated ER stress and corrected LPS-induced calcium overloading. Besides, MKP1 adenovirus transfection also reversed mitochondrial bioenergetics, maintained mitochondrial membrane potential, and blocked mitochondria-initiated apoptosis signals. Furthermore, we found that MKP1 overexpression is associated with inactivation of mitogen-activated protein kinase-c-Jun N-terminal kinase (MAPK-JNK) pathway. Interestingly, the activation of MAPK-JNK pathway could abolish the protective effects of MKP1 on BV-2 cells survival and mitochondrial function in the presence of LPS. Altogether, our results identified MKP1 as a primary defender of neuroinflammation via modulating ER stress and mitochondrial function in a manner dependent on MAPK-JNK pathway. These findings may open a new window for the treatment of neuroinflammation in the clinical setting. K E Y W O R D S BV-2 cells, ER stress, LPS, mitochondrial damage, MKP1, neuroinflammation

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The lncRNA HOTAIR transcription is controlled by HNF4α-induced chromatin topology modulation

Cited by 64 publications

References 45 publications

Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

Control of Cell Identity by the Nuclear Receptor HNF4 in Organ Pathophysiology

MKP1 reduces neuroinflammation via inhibiting endoplasmic reticulum stress and mitochondrial dysfunction

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