Knockdown of long non-coding RNA HOTAIR inhibits proliferation and invasiveness and improves radiosensitivity in colorectal cancer

Yang, Xiaodong; Xu, Hong‐Tao; Xu, Xiaohui; Ru, Gan; Liu, Wei; Zhu, Jinming; Wu, Yongyou; Zhao, Kui; Wu, Yong; Zhang, Shuyu; Cao, Jianping; Li, Ming

doi:10.3892/or.2015.4397

Cited by 80 publications

(56 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Abnormal expression lncRNAs could serve as oncogenes and tumor suppressors, closely associated with tumorigenesis, metastasis, prognosis or diagnosis [15]. Moreover, accumulating documents reveal that lncRNAs are related to radiotherapy resistance of cancers [16–18]. For instance, HOTAIR expression was upregulated in tumor tissues of colorectal cancer (CRC) patients, and HOTAIR knockdown inhibited proliferation, migration and invasiveness while enhanced apoptosis and radiosensitivity of CRC cells [18].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, accumulating documents reveal that lncRNAs are related to radiotherapy resistance of cancers [16–18]. For instance, HOTAIR expression was upregulated in tumor tissues of colorectal cancer (CRC) patients, and HOTAIR knockdown inhibited proliferation, migration and invasiveness while enhanced apoptosis and radiosensitivity of CRC cells [18]. HOTAIR expression was markedly increased in the pancreatic ductal adenocarcinoma (PDAC) cell lines and tissues, and HOTAIR silencing improved the radiosensitivity of PDAC cells via regulating the expression of Wnt inhibitory factor 1 (WIF-1) [16].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression

Jiang

Zhang

et al. 2017

Radiat Oncol

View full text Add to dashboard Cite

BackgroundLong non-coding RNAs (lncRNAs) have been reported to regulate the sensitivity of different cancer cells to chemoradiotherapy. Aberrant expression of lncRNA Taurine-upregulated gene 1 (TUG1) has been found to be involved in the development of bladder cancer, however, its function and underlying mechanism in the radioresistance of bladder cancer remains unclear.MethodsQuantitative real-time PCR (qRT-PCR) was conducted to measure the expression of TUG1 and HMGB1 mRNA in bladder cancer tissues and cell lines. HMGB1 protein levels were tested by western blot assays. Different doses of X-ray were used for radiation treatment of bladder cancer cells. Colony survival and cell viability were detected by clonogenic assay and CCK-8 Kit, respectively. Cell apoptosis was determined by flow cytometry. A xenograft mouse model was constructed to observe the effect of TUG1 on tumor growth in vivo.ResultsThe levels of TUG1 and HMGB1 were remarkably increased in bladder cancer tissues and cell lines. Radiation treatment markedly elevated the expression of TUG1 and HMGB1. TUG1 knockdown inhibited cell proliferation, promoted cell apoptosis and decreased colony survival in SW780 and BIU87 cells under radiation. Moreover, TUG1 depletion suppressed the HMGB1 mRNA and protein levels. Furthermore, overexpression of HMGB1 reversed TUG1 knockdown-induced effect in bladder cancer cells. Radiation treatment dramatically reduced the tumor volume and weight in xenograft model, and this effect was more obvious when combined with TUG1 silencing.ConclusionLncRNA TUG1 knockdown enhances radiosensitivity of bladder cancer by suppressing HMGB1 expression. TUG1 acts as a potential regulator of radioresistance of bladder cancer, and it may represent a promising therapeutic target for bladder cancer patients.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression

Jiang

Zhang

et al. 2017

Radiat Oncol

View full text Add to dashboard Cite

show abstract

“…Reduced levels of HOTAIR expression led to a decrease in the survival of human CRC stem cells, and knockdown of HOTAIR suppressed CRC proliferation, colony formation, migration, and invasion. In particular, downregulation of HOTAIR expression improved radiosensitivity in CRC [88,89]. One major reason for the failure of CRC treatment is the occurrence of chemoresistance; silencing of HOTAIR reversed fluoropyrimidinebased chemoresistance by increasing miR-218 expression and inactivating transcription factor nuclear factor-kappaB (NF-κB) signaling.…”

Section: Hotair In Colorectal Cancermentioning

confidence: 99%

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

Tang

Hann

2018

Cell Physiol Biochem

219

135

View full text Add to dashboard Cite

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.

show abstract

“…For example, Yang et al implied that knockdown of lncRNA HOX transcript antisense intergenic RNA (HOTAIR) contributed to tumorigenesis and enhanced radiosensitivity of CRC [32]. Lu et al exhibited that high expression of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) regulated radioresistance through modulating mesenchymal transition (EMT) [33].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195

Zhang

et al. 2017

Cell Physiol Biochem

111

View full text Add to dashboard Cite

Background/Aims: Plasmacytoma variant translocation 1 (PVT1) exerts an oncogenic role in many tumors, including lung cancer. However, the roles of PVT1 in regulating radiosensitivity of NSCLC and its underlying mechanism are still unclear. Methods: Expression levels of PVT1 and miR-195 in NSCLC tissues and cells were examined by qRT-PCR. Effects of PVT1 and miR-195 on cell proliferation, apoptosis and colony formation abilities were assessed by MTT assay, flow cytometry and colony formation assay. Luciferase reporter assay was performed to confirm the relationship between PVT1 and miR-195. Tumor xenograft experiments were conducted to observe the effect of PVT1 on radiosensitivity of NSCLC in vivo. Results: PVT1 was negatively correlated with miR-195 expression in NSCLC tissues and associated with poor prognosis of NSCLC patients. Expression of PVT1 and miR-195 varied inversely after irradiation in NSCLC cells. PVT1 knockdown or miR-195 overexpression enhanced radiosensitivity of NSCLC in vitro by inhibiting proliferation and inducing apoptosis. PVT1 directly interacted with miR-195 and regulated its expression. Moreover, PVT1 knockdown improved radiosensitivity of NSCLC cells in vitro and in vivo by sponging miR-195. Conclusion: Knockdown of PVT1 enhances radiosensitivity of NSCLC by sponging miR-195, providing a novel therapeutic target to improve radiotherapy efficiency in NSCLC.

show abstract

Knockdown of long non-coding RNA HOTAIR inhibits proliferation and invasiveness and improves radiosensitivity in colorectal cancer

Cited by 80 publications

References 34 publications

Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression

Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression

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

Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195

Contact Info

Product

Resources

About