HOTAIR enhanced aggressive biological behaviors and induced radio-resistance via inhibiting p21 in cervical cancer

Li, Jing; Wang, Yuan; Dong, Ruofan; Yu, Jinjin; Qiu, Haifeng

doi:10.1007/s13277-014-2998-2

Cited by 96 publications

(74 citation statements)

References 32 publications

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“…Many lncRNAs emerged as pivotal regulators in various biological processes and played important roles in oncogenesis and progression of CaCx [92]. High HOTAIR expression in CaCx was significantly correlated with progression and poor prognosis, and elevated HOTAIR expression could induce radioresistance by inhibiting p21; this finding indicates that targeting HOTAIR is a potential therapeutic strategy in CaCx [93]. HOTAIR expression in the sera was significantly increased in patients with CaCx relative to that in normal controls.…”

Section: Hotair In Cervical Cancermentioning

confidence: 96%

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

Tang

Hann

2018

Cell Physiol Biochem

204

127

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Long non-coding RNAs (LncRNAs) represent a novel class of noncoding RNAs that are longer than 200 nucleotides without protein-coding potential and function as novel master regulators in various human diseases, including cancer. Accumulating evidence shows that lncRNAs are dysregulated and implicated in various aspects of cellular homeostasis, such as proliferation, apoptosis, mobility, invasion, metastasis, chromatin remodeling, gene transcription, and post-transcriptional processing. However, the mechanisms by which lncRNAs regulate various biological functions in human diseases have yet to be determined. HOX antisense intergenic RNA (HOTAIR) is a recently discovered lncRNA and plays a critical role in various areas of cancer, such as proliferation, survival, migration, drug resistance, and genomic stability. In this review, we briefly introduce the concept, identification, and biological functions of HOTAIR. We then describe the involvement of HOTAIR that has been associated with tumorigenesis, growth, invasion, cancer stem cell differentiation, metastasis, and drug resistance in cancer. We also discuss emerging insights into the role of HOTAIR as potential biomarkers and therapeutic targets for novel treatment paradigms in cancer.

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Section: Hotair In Cervical Cancermentioning

confidence: 96%

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

Tang

Hann

2018

Cell Physiol Biochem

204

127

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“…Of note, a microarray analysis confirmed that lncRNAs HOX antisense intergenic RNA (HOAIR), CCAT1 and HIF1A‐AS1 were over‐expressed within retinoblastoma tissues, yet lncRNAs MIR31HG, BCAR4 and H193 were evidently under‐expressed within retinoblastoma tissues 13. Among them, HOTAIR was identified to be a cis‐acting parameter within the HOXC loca,14, 15, 16 and its carcinogenicity has been authenticated within breast cancer, liver cancer, colorectal cancer, oesophageal squamous cancer, pancreatic cancer, non‐small cell lung cancer and cervical cancer 17, 18, 19, 20, 21, 22, 23, 24. In addition, HOAIR was indicated as a potential therapeutic biomarker for retinoblastoma, and silencing of HOTAIR could attenuated proliferation, migration and invasion of retinoblastoma cells were determined after 25…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Yang

et al. 2018

J Cellular Molecular Medi

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Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR‐613 and c‐met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour‐adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO‐Rb44, SO‐Rb50 and WERI‐RB1) were also gathered. Moreover, transfections of pcDNA3.1‐HOTAIR, si‐HOTAIR, miR‐613 mimic, miR‐613 inhibitor, pcDNA3.1/c‐met were performed to evaluate the influence of HOTAIR, miR‐613 and c‐met on viability, apoptosis and epithelial‐mesenchymal transition (EMT) of retinoblastoma cells. Dual‐luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR‐613, as well as between miR‐613 and c‐met. Consequently, up‐regulated HOTAIR and down‐regulated miR‐613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR‐613 elevated E‐cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less‐motivated (P < 0.05). Nonetheless, c‐met prohibited the functioning of miR‐613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR‐613, and c‐met was the direct target gene of miR‐613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR‐613/c‐met signalling axis in modulating retinoblastoma cells’ viability, apoptosis and expressions of EMT‐specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.

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“…In cervical cancer, many LncRNAs have been found to suppress metastasis, as well as help in the prediction of metastasis through their expression levels (15). HOX transcript antisense intergenic RNA (HOTAIR) has been identified as an upregulated LncRNA in cervical cancer (16), and a recent study has revealed that HOTAIR enhanced aggressive biological behavior and induced radio-resistance via inhibiting p21 in cervical cancer, which proposed that targeting HOTAIR might be a potent therapeutic strategy in cervical cancer, especially for those patients who were administered radiotherapy (17). However, little is known about the overall biological role of HOTAIR in cervical cancer, or the underlying molecular mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer

Sun

Chu

et al. 2016

International Journal of Oncology

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Abstract. The long non-coding RNA HOX transcript antisense RNA (HOTAIR) has been found overexpressed in many human malignancies and involved in tumor progression and metastasis. However, little is known about the potential biological roles of HOTAIR in tumor escape. In the present study, the expression of HOTAIR was detected in 59 paired cervical cancer tissue samples by real-time PCR and then subjected to correlation analysis with clinical features. The effects of HOTAIR on cervical cancer cells as well as the expression of human leukocyte antigen (HLA)-G were studied by overexpression and RNA interference approaches. Insight into the mechanism of HOTAIR acting as competitive endogenous RNAs (ceRNAs) was gained from bioinformatic analysis and luciferase assays. HOTAIR expression was obviously increased in cervical cancer tissue. HOTAIR upregulation was associated with advanced pathological stage, histology, lymph node invasion and lymphatic metastasis, and also correlated with shorter overall survival of cervical cancer patients. Furthermore, HOTAIR overexpression promoted the proliferation, migration and invasion of cervical cancer cells, while HOTAIR knockdown inhibited cell invasion and cell viability, induced apoptosis and inhibited growth in vitro and in vivo. Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a. Our data suggest that HOTAIR plays an important oncogenic role in cervical cancer and might serve as a marker for cervical cancer prognosis and a potential target for therapeutic intervention.

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HOTAIR enhanced aggressive biological behaviors and induced radio-resistance via inhibiting p21 in cervical cancer

Cited by 96 publications

References 32 publications

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer

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