LncRNA MALAT1 is up-regulated in diabetic gastroparesis and involved in high-glucose-induced cellular processes in human gastric smooth muscle cells

Gong, Yuhan; Zhu, Ying; Zhu, Bingqian; Si, Xiaoyan; Heng, Ding; Tang, Yurong; Sun, Xiaomeng; Lin, Lin

doi:10.1016/j.bbrc.2018.01.038

Cited by 14 publications

(28 citation statements)

References 28 publications

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“…Previous study has revealed that apoptosis of CEP cells induced by high glucose contributes to idd (12). MalaT1 plays an essential role in a number of diabetes-related complications (20)(21)(22)(23)(24). However, the role of MALAT1 in diabetes-associated idd has not been determined.…”

Section: Discussionmentioning

confidence: 99%

“…recent studies have revealed that MalaT1 contributes to certain diabetes-related complications, including cerebral ischaemic reperfusion injury, atherosclerosis, cataracts, retinopathy, cardiomyopathy, gastropathy and kidney disease. it has been reported that the expression of MALAT1 is upregulated in multiple cells and tissues in patients and animals with diabetes (20)(21)(22)(23)(24). Increased MALAT1 expression is an important reason for the initiation and development of diabetes-related diseases.…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, studies have revealed that MalaT1 also plays an important role in diabetes-related complications. it has been reported that MalaT1 contributes to certain diabetes-related complica-tions, including cataracts, retinopathy, cardiomyopathy, gastropathy and kidney disease (19)(20)(21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

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Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Jiang

Zeng

et al. 2020

Mol Med Report

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diabetes mellitus (dM) contributes to intervertebral disc degeneration (idd). The long non-coding rna MalaT1 has been revealed to play an important role in diabetes-associated complications. However, the specific role of MALAT1 in diabetes-associated idd has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. rat ceP cells were cultured in high-glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription-quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MalaT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying idd in patients with diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Jiang

Zeng

et al. 2020

Mol Med Report

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“…An increasing number of studies have focused on the involvement of non-coding RNAs in HSCC with the aim of identifying possible therapeutic strategies (3,4). Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding (lnc)RNA that has been reported to be involved in neurogenesis (5), metabolic (6) and vascular (7,8) diseases, as well as certain types of cancer (9). MALAT1 affects neuronal differentiation by activating the ERK and mitogen-activated protein kinase (MAPK) signaling pathway in neuro-2a cells (5).…”

Section: Introductionmentioning

confidence: 99%

“…MALAT1 affects neuronal differentiation by activating the ERK and mitogen-activated protein kinase (MAPK) signaling pathway in neuro-2a cells (5). MALAT1 has also been reported to be upregulated in a rat model of diabetic gastroparesis, which increases the expression of α-smooth muscle actin and smooth muscle myosin heavy chains, and promotes the apoptosis of human gastric smooth muscle cells (6). A previous study also revealed that MALAT1 knockdown inhibited ischemic injury and autophagy by targeting miR-30a in vitro and in vivo (7).…”

Section: Introductionmentioning

confidence: 99%

MALAT1 knockdown inhibits hypopharyngeal squamous cell carcinoma malignancy by targeting microRNA‑194

Wang

Ouyang

et al. 2020

Oncol Lett

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the oncogenesis and progression of various types of cancer. However, the function of MALAT1 in hypopharyngeal squamous cell carcinoma (HSCC) is not completely understood. In the present study, MALAT1 expression levels were determined using reverse transcription-quantitative PCR, and Cell Counting Kit-8, Transwell and flow cytometry assays were performed to investigate the biological functions of HSCC cells. The results indicated that MALAT1 was upregulated in HSCC. MALAT1 knockdown suppressed HSCC cell proliferation, migration and invasion, and promoted apoptosis compared with the control group. Additionally, microRNA (miR)-194 was identified as a target of MALAT1 and was expressed at low levels in HSCC tissues compared with adjacent non-tumor tissues. A miR-194 agomir inhibited malignant cell behaviors, including cell proliferation, migration and invasion, whereas miR-194 antagomir promoted malignant behaviors compared with the corresponding control groups. In addition, the results suggested that MALAT1 knockdown inhibited the malignant behaviors of HSCC cells by binding miR-194. miR-194 inhibition partially reversed the MALAT1 knockdown-induced inhibitory effects on HSCC cells. Furthermore, MALAT1 knockdown combined with miR194 mimics resulted in the lowest tumor volume among all tested groups in vivo. In conclusion, the results of the present study suggested that MALAT1 knockdown suppressed the malignant behavior of HSCC by targeting miR-194; therefore, MALAT1 may serve as a novel therapeutic target for HSCC.

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miR‐449a: A Promising Biomarker and Therapeutic Target in Cancer and Other Diseases

Barati,

Mirzaei,

Ebrahimi

et al. 2024

Cell Biochem Biophys

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LncRNA MALAT1 is up-regulated in diabetic gastroparesis and involved in high-glucose-induced cellular processes in human gastric smooth muscle cells

Cited by 14 publications

References 28 publications

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

MALAT1 knockdown inhibits hypopharyngeal squamous cell carcinoma malignancy by targeting microRNA‑194

miR‐449a: A Promising Biomarker and Therapeutic Target in Cancer and Other Diseases

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