Dataset Information

LncRNA XIST regulates cell proliferation, migration and invasion via regulating miR-30b and RECK in nasopharyngeal carcinoma.

ABSTRACT: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) plays an essential role in the development and progress of nasopharyngeal carcinoma (NPC). MicroRNA-30b (miR-30b) has been confirmed to play an inhibitory role in various types of cancer. The molecular mechanisms underlying the lncRNA XIST-mediated regulation of the metastasis of NPC cells by miR-30b is not clear. qPCR and western blot analysis were used to detect the expression of XIST, miR-30b, and reversion inducing cysteine rich protein with kazal motifs (RECK) in NPC tissues and cell lines. The detection of luciferase reporter gene confirmed the relationship between lncRNA XIST, miR-30b and RECK. CCK-8 and Transwell assays were performed in order to detect the proliferation, migration and invasion of the NPC cells. The results of qPCR and western blotting indicated that the expression levels of lncRNA XIST and RECK were higher in the NPC tissues and cell lines than that of the control group, while the expression of miR-30b was lower. Knockdown of lncRNA XIST significantly inhibited cell proliferation, migration and invasion in the NPC cell lines. In addition, lncRNA XIST was found to negatively regulate the expression of miR-30b, resulting in the upregulation of RECK. Overexpression of RECK was found to reverse the inhibitory effect of lncRNA XIST knockdown or miR-30b on NPC cell metastasis. Our results showed that cell migration and invasion were inhibited by knockdown of lncRNA XIST, suggesting that the lncRNA XIST/miR-30b/RECK axis is involved in the development of NPC.

SUBMITTER: Sun L

PROVIDER: S-EPMC7882881 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

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lncRNA XIST regulates cell proliferation, migration and invasion via regulating miR-30b and RECK in nasopharyngeal carcinoma.

Sun Lingling L Zhang Min M Qu Hongxia H

Oncology letters 20210204 4

Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) plays an essential role in the development and progress of nasopharyngeal carcinoma (NPC). MicroRNA-30b (miR-30b) has been confirmed to play an inhibitory role in various types of cancer. The molecular mechanisms underlying the lncRNA XIST-mediated regulation of the metastasis of NPC cells by miR-30b is not clear. qPCR and western blot analysis were used to detect the expression of XIST, miR-30b, and reversion inducing cysteine r ...[more]

PMID: 33664820

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Project description:Centromere coiled-coil protein 110 (CCP110) plays a role in the development of several types of cancer; however, its regulatory mechanism and role in endometrial cancer is unclear. The present study revealed that CCP110 is regulated by a signaling pathway involving microRNA (miR/miRNA)-129-2-3p and the long non-coding RNA (lncRNA) X-inactive-specific transcript (XIST), and plays a role in controlling the proliferation, migration and invasion of endometrial cancer cells. CCP110 was upregulated in human endometrial cancer tissues, as revealed by immunohistochemistry, and high expression of the protein was related to reduced overall survival of the patients. Genetic knockdown of CCP110 by small interfering RNA promoted apoptosis and suppressed the proliferation, migration, invasion and colony formation of endometrial cancer cells significantly in the endometrial cancer Ishikawa and HEC-1B cell lines, as assessed by flow cytometry, and Cell Counting Kit-8, Transwell and colony formation assays. A bioinformatics analysis and luciferase reporter assay revealed that CCP110 is a target of miR-129-2-3p. Overexpression of miR-129-2-3p mimic fragments inhibited the proliferation, migration and invasion of endometrial cancer cells significantly, while co-overexpression of CCP110 counteracted these inhibitory effects. The expression level of the lncRNA XIST was upregulated significantly in endometrial cancer tissues, as assessed by reverse transcription-quantitative PCR assay, while that of miR-129-2-3p was downregulated significantly. A bioinformatics analysis and luciferase reporter assay showed that XIST could inhibit miR-129-2-3p via a miRNA sponge effect. Furthermore, co-overexpression of XIST antagonized the inhibitory effect of the miR-129-2-3p mimic on the luciferase reporter gene signal and protein expression of CCP110. Co-overexpression of XIST also abolished the inhibitory effect of the miR-129-2-3p mimic on the proliferation, migration and invasion of endometrial cancer cells. Overall, these data identified a novel regulatory mechanism of CCP110 involving XIST and miR-129-2-3p, which affected the development of endometrial carcinoma. CCP110, XIST and miR-129-2-3p could represent novel targets for the clinical treatment of endometrial cancer.

Project description:The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR-663b. It was demonstrated that miR-663b was significantly upregulated in NPC tissue compared with non-tumor nasopharyngeal epithelial tissue samples. Furthermore, miR-663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR-663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR-663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR-663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR-663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR-663b negatively regulated the expression of TUSC2 at the post-transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR-663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR-663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR-663b is a promising therapeutic target for the treatment of patients with NPC.

Dataset Information

LncRNA XIST regulates cell proliferation, migration and invasion via regulating miR-30b and RECK in nasopharyngeal carcinoma.

Publications

lncRNA XIST regulates cell proliferation, migration and invasion via regulating miR-30b and RECK in nasopharyngeal carcinoma.

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