Long non‐coding RNA HOTAIR/microRNA‐206 sponge regulates STC2 and further influences cell biological functions in head and neck squamous cell carcinoma

Li, Tiancheng; Yao, Qing; Zhen, Zhen; Shen, Hong; Cong, Tiechuan; Schiferle, Erik; Xiao, Shuai

doi:10.1111/cpr.12651

Cited by 49 publications

(40 citation statements)

References 38 publications

(70 reference statements)

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“…LncRNAs were proved to take part in the regulation of several biological processes such as cell proliferation, apoptosis, migration, and invasion in a variety of diseases or tumors [11,12]. Long noncoding RNA HOTAIR was reported to accelerate the proliferation, migration, and invasion of head and neck squamous cell carcinoma (HNSCC) cells by sponging microRNA-206 and targeting STC2 [13]. Additionally, long noncoding RNA ZFAS1 facilitated chondrocytes proliferation, migration, and apoptosis of in osteoarthritis [14].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Yang

Lin

2020

Cardiovascular Therapeutics

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Background. Myocardial infarction (MI) was a severe cardiovascular disease resulted from acute, persistent hypoxia, or ischemia condition. Additionally, MI generally led to heart failure, even sudden death. A multitude of research studies proposed that long noncoding RNAs (lncRNAs) frequently participated in the regulation of heart diseases. The specific function and molecular mechanism of SOX2-OT in MI remained unclear. Aim of the Study. The current research was aimed to explore the role of SOX2-OT in MI. Methods. Bioinformatics analysis (DIANA tools and Targetscan) and a wide range of experiments (CCK-8, flow cytometry, RT-qPCR, luciferase reporter, RIP, caspase-3 activity, trans-well, and western blot assays) were adopted to investigate the function and mechanism of SOX2-OT. Results. We discovered that hypoxia treatment decreased cell viability but increased cell apoptosis. Besides, lncRNA SOX2-OT expression was upregulated in hypoxic HCMs. Hereafter, we confirmed that SOX2-OT could negatively regulate miR-27a-3p levels by directly binding with miR-27a-3p, and miR-27a-3p also could negatively regulate SOX2-OT levels. Furthermore, knockdown of SOX2-OT promoted cell proliferation, migration, and invasion, but limited cell apoptosis. However, these effects were reversed by anti-miR-27a-5p. Besides, we verified that miR-27a-3p binding with the 3′UTR of TGFBR1 and SOX2-OT regulated TGFβR1 level by collaborating with miR-27a-3p in HCMs. Eventually, rescue assays validated that the influence of SOX2-OT silence or miR-27a-3p overexpression on cellular processes in cardiomyocytes injury was counteracted by TGFBR1 overexpression. Conclusions. Long noncoding RNA SOX2-OT exacerbated hypoxia-induced cardiomyocytes injury by regulating miR-27a-3p/TGFβR1 axis, which may provide a novel insight for heart failure treatment.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Yang

Lin

2020

Cardiovascular Therapeutics

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“…The early one in the three was to identify HOTAIR sponging miR-206 could activate bcl-w to facilitate the cell proliferation [35]. The following researches confirmed that HOTAIR negatively regulated miR-206 to activate STS2 [33] to promote cancer invasion of head and neck squamous cell carcinoma as well as to activate CCND1 and CCND2 [34] to stimulate the proliferation, and invasion of ovarian cancer cells. It is meaningful to explore the HOTAIR/miR-206 axis in CRC.…”

Section: Discussionmentioning

confidence: 99%

“…It's interesting that we verified HOTAIR could act as a competitive endogenous to sponge miR-206 to enhance ability of proliferation and invasion in CRC cells. There are three studies in head and neck squamous cell carcinoma [33], ovarian cancer [34], breast cancer [35] but CRC focusing on the repressing role of HOTAIR to sponge miR-206. The early one in the three was to identify HOTAIR sponging miR-206 could activate bcl-w to facilitate the cell proliferation [35].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HOTAIR as a competitive endogenous RNA to sponge miR-206 to promote colorectal cancer progression by activating CCL2

Jia¹,

Xie²,

Jin³

et al. 2020

J. Cancer

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Colorectal cancer (CRC) is one of the common malignant tumors, the incidence of which is on rise. LncHOTAIR, considered as an oncogene, contributed to the progression of a lot of cancers. However, the molecular mechanism and biological functions of the HOTAIR/miR-206/CCL2 axis have not been reported before. Here, our research aimed to explore HOTAIR/miR-206/CCL2 axis in CRC to demonstrate its role in predicting the poor prognosis of CRC. LncHOTAIR, miR-206 and CCL2 mRNA were detected in CRC tissues and cells by RT-PCR. The interactions among LncHOTAIR, miR-206 and CCL2 were explored by luciferase reporter assay, qRT-PCR, western blot and RNA interfere. Flow Cytometry Cell Analysis was performed to detect cell cycle and apoptosis as well as colony assay was prepared to test the cell proliferation. Immunohistochemical analysis was used to detect the CCL2 protein in CRC tissues. In our study, silence of LncHOTAIR by RNA interference could suppress the proliferation, migration and invasion of CRC cells. Mechanistically, LncHOTAIR downregulated miR-206 abundance which indicated that LncHOTAIR was considered as a competing endogenous RNA (ceRNA) by directly sponging miR-206 in CRC cells. In addition, further exploration suggested that miR-206 could inhibit the function of the downstream CCL2, the expression of which was repressed by LncHOTAIR/miR-206 signaling. Furthermore, we verified that the overexpression of CCL2 attenuated CRC cell proliferation, migration, invasion. Overall, this study firstly elucidated that LncHOTAIR played as oncogene in CRC via directly sponging miR-206 to activate the downstream CCL2, which would be considered as the novel therapeutic target in CRC.

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“…HOTAIR can competitively decoy miRNA from messenger RNA (mRNA) and release its inhibitory effect on mRNA. 96,97 Subsequently, the invasion, metastasis, escape of growth inhibition, and apoptosis of cancer cells are affected, which may be the leading cause of poor survival. 97…”

Section: Micrornamentioning

confidence: 99%

Emerging roles of HOTAIR in human cancer

Yuan

Ning

Pan

2020

J of Cellular Biochemistry

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Long noncoding RNA HOX antisense intergenic RNA (HOTAIR) is overexpressed in many types of cancers, and substantial evidence has suggested a link between cancers and HOTAIR. In the present study, we reviewed the structure and the corresponding biologic function of HOTAIR to clarify its molecular mechanism in cancer progression. HOTAIR promotes proliferation, invasion, and migration, and inhibits apoptosis in cancer cells. HOTAIR also participates in the pathogenesis and progression of cancer by regulating inflammation and immune signaling. These findings suggested that HOTAIR is a novel biomarker in human cancers. K E Y W O R D S biomarker, epithelial-mesenchymal transformation, HOTAIR, immune signaling, nasopharyngeal carcinoma

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Long non‐coding RNA HOTAIR/microRNA‐206 sponge regulates STC2 and further influences cell biological functions in head and neck squamous cell carcinoma

Cited by 49 publications

References 38 publications

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

Long non-coding RNA HOTAIR as a competitive endogenous RNA to sponge miR-206 to promote colorectal cancer progression by activating CCL2

Emerging roles of HOTAIR in human cancer

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