Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p

Yuan Donglan; Zhu Dandan; Yin Boyu; Ge Hongshan; Zhao Yinling; Huang Aihua; Wang Xiaosu; Cao Xiuhong; Xia Nan; Qian Hua

doi:10.1007/s13258-021-01184-y

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자료유형: 학술저널

저자정보: Yuan Donglan (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Zhu Dandan (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Yin Boyu (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Ge Hongshan (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Zhao Yinling (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Huang Aihua (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Wang Xiaosu (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Cao Xiuhong (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Xia Nan (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China) Qian Hua (Taizhou People‘s Hospital Affiliated to Nantong University People’s Republic of China)

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.44 No.5

발행연도: 2022.5

수록면: 527 - 537 (11page)

DOI: 10.1007/s13258-021-01184-y

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Background Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear. Objective This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM. Methods Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays. Results MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p. Conclusions NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.

Background Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear. Objective This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM. Methods Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays. Results MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p. Conclusions NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.

#Long non-coding cRNA NEAT1 · microRNA-124-3p · Endometriosis · Eutopic endometrium · Autotransplantation

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