Dataset Information

LncRNA FEZF1-AS1 Promotes TGF-?2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.

ABSTRACT: Posterior capsule opacification (PCO) is a common complication after cataract surgery attributed to the proliferation and migration of postoperative residual lens epithelial cells (LECs). The long noncoding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) promotes the proliferation and migration of multiple types of cancer cells. Here, we discovered that FEZF1-AS1 is markedly upregulated in TGF-?2-treated SRA01/04?cells. In addition, the proliferation and migration of SRA01/04?cells were enhanced following TGF-?2 treatment. FEZF1-AS1 knockdown inhibited the TGF-?2-induced proliferation and migration of SRA01/04?cells. Accordingly, FEZF1-AS1 overexpression promoted the TGF-?2-induced proliferation and migration of SRA01/04?cells. Finally, FEZF1-AS1 upregulated TGF-?2-induced SRA01/04?cell proliferation and migration via boosting FEZF1 protein levels. Our findings indicate that the dysregulation of FEZF1-AS1 participates in the TGF-?2-induced proliferation and migration of human lens epithelial cells (HLECs), which might be achieved, at least in part, through the induction of FEZF1 expression.

SUBMITTER: Wang Y

PROVIDER: S-EPMC6594282 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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LncRNA FEZF1-AS1 Promotes TGF-<i>β</i>2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.

Wang Yong Y Chen Lili L Gu Yonghui Y Wang Ying Y Yuan You Y Zhu Qiujian Q Bi Mingchao M Gu Shuyan S

Journal of ophthalmology 20190612

Posterior capsule opacification (PCO) is a common complication after cataract surgery attributed to the proliferation and migration of postoperative residual lens epithelial cells (LECs). The long noncoding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) promotes the proliferation and migration of multiple types of cancer cells. Here, we discovered that FEZF1-AS1 is markedly upregulated in TGF-<i>β</i>2-treated SRA01/04 cells. In addition, the proliferation and migration of SRA ...[more]

PMID: 31281667

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Project description:BackgroundBladder cancer is the most common human urological malignancies with poor prognosis, and the pathophysiology of bladder cancer involves multi-linkages of regulatory networks in the bladder cancer cells. Recently, the long noncoding RNAs (lncRNAs) have been extensively studied for their role on bladder cancer progression. In this study, we evaluated the expression of DLX6 Antisense RNA 1 (DLX6-AS1) in the cancerous bladder tissues and studied the possible mechanisms of DLX6-AS1 in regulating bladder cancer progression.MethodsGene expression was determined by qRT-PCR; protein expression levels were evaluated by western blot assay; in vitro functional assays were used to determine cell proliferation, invasion and migration; nude mice were used to establish the tumor xenograft model.ResultsOur results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis. The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells. Further results showed that DLX6-AS1 overexpression increased the activity of Wnt/?-catenin signaling, and the oncogenic role of DLX6-AS1 in bladder cancer cells was abolished by the presence of XAV939. On the other hand, DLX6-AS1 knockdown suppressed the activity of Wnt/?-catenin signaling, and the tumor-suppressive effects of DLX6-AS1 knockdown partially attenuated by lithium chloride and SB-216763 pretreatment. The in vivo tumor growth study showed that DLX6-AS1 knockdown suppressed tumor growth of T24 cells and suppressed EMT and Wnt/?-catenin signaling in the tumor tissues.ConclusionCollectively, the present study for the first time identified the up-regulation of DLX6-AS1 in clinical bladder cancer tissues and in bladder cancer cell lines. The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/?-catenin signaling pathway.

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Dataset Information

LncRNA FEZF1-AS1 Promotes TGF-?2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.

Publications

LncRNA FEZF1-AS1 Promotes TGF-<i>β</i>2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.

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