Overexpression of long non-coding RNA HOTAIR leads to chemoresistance by activating the Wnt/β-catenin pathway in human ovarian cancer

Li, Jing; Yang, Siqin; Su, Ning; Wang, Yuan; Yu, Jinjin; Qiu, Haifeng; He, Xiaoyun

doi:10.1007/s13277-015-3998-6

Cited by 178 publications

(177 citation statements)

References 24 publications

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“…Interaction with kinases, such as mitogen-activated protein kinase 1 (MAPK1), regulated the growth, migration, and invasion of OC cells [108]. Overexpression of HOTAIR promoted the progression, proliferation, and chemoresistance of the cell cycle by activating the Wnt/β-catenin pathway in OC cells [109]. In one study, a peptide nucleic acid (PNA)-based approach was found to hinder the interaction of HOTAIR with EZH2, inhibiting the HOTAIR-EZH2 associated pathway and re-sensitized resistant OC to platinum; treatment of OC cells with overexpressed HOTAIR with PNAs decreased invasiveness and increased chemosensitivity, which were correlated with reduced activation and decreased expression of the NF-κB target genes MMP-9 and interleukin 6.…”

Section: Hotair In Ovarian Cancermentioning

confidence: 99%

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

Tang

Hann

2018

Cell Physiol Biochem

213

135

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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 Ovarian Cancermentioning

confidence: 99%

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

Tang

Hann

2018

Cell Physiol Biochem

213

135

View full text Add to dashboard Cite

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“…The study showed that higher expression of HOTAIR in OC cells induced cisplatin resistance through upregulation of the Wnt/b-catenin signaling pathway and promoting cell cycle progression. Conversely, inhibition of HOTAIR resulted in cisplatin sensitivity, in vitro and in vivo by suppressing Wnt/b-catenin signaling and inducing cell cycle arrest at G1 phase [119]. A recent study performed by Ozes and collogues revealed that HOTIAR mediates chemoresistance in DNA-damage responses through the NF-κB signaling pathway [41].…”

Section: Lncrnas and Partner Molecules Mediate Drug-resistance In Ocmentioning

confidence: 99%

Long Non-Coding RNAs: the New Horizon of Gene Regulation in Ovarian Cancer

Worku

Bhattarai

Ayers

et al. 2017

Cell Physiol Biochem

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Long non-coding RNAs (lncRNAs), a class of non-coding transcripts, have recently been emerging with heterogeneous molecular actions, adding a new layer of complexity to generegulation networks in tumorigenesis. LncRNAs are considered important factors in several ovarian cancer histotypes, although few have been identified and characterized. Owing to their complexity and the lack of adapted molecular technology, the roles of most lncRNAs remain mysterious. Some lncRNAs have been reported to play functional roles in ovarian cancer and can be used as classifiers for personalized medicine. The intrinsic features of lncRNAs govern their various molecular mechanisms and provide a wide range of platforms to design different therapeutic strategies for treating cancer at a particular stage. Although we are only beginning to understand the functions of lncRNAs and their interactions with microRNAs (miRNAs) and proteins, the expanding literature indicates that lncRNA-miRNA interactions could be useful biomarkers and therapeutic targets for ovarian cancer. In this review, we discuss the genetic variants of lncRNAs, heterogeneous mechanisms of actions of lncRNAs in ovarian cancer tumorigenesis, and drug resistance. We also highlight the recent developments in using lncRNAs as potential prognostic and diagnostic biomarkers. Lastly, we discuss potential approaches for linking lncRNAs to future gene therapies, and highlight future directions in the field of ovarian cancer research.

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“…Though initially sensitive to chemotherapy, up to 80% of patients with ovarian cancer produce endogenous or acquired chemoresistance (1). The recurrence and metastasis of ovarian cancer results in poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

53BP1 inhibits the migration and regulates the chemotherapy resistance of ovarian cancer cells

Hong

Zhao

et al. 2018

Oncol Lett

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Abstract. The major problems faced during the treatment of ovarian cancer are metastasis and the development of intrinsic or acquired drug resistance. The present study assessed whether tumor protein p53 binding protein 1 (53BP1) regulated migration and modulated chemotherapy resistance in SKOV3 cells and identified proteins associated with the molecular mechanisms underlying this coordinate regulation. SKOV3 cells were transfected using a 53BP1-expressing vector, which induced 53BP1 overexpression. The migration of the transfected cells was observed using a Transwell assay. The expression of matrix metalloproteinase (MMP)-2 and MMP-9 were assayed using gelatin zymography. In addition, the effects of 53BP1 on the chemosensitivity of SKOV3 cells to cisplatin were evaluated using MTT and western blot assays. Compared with the control, the average number of migrating SKOV3/pLPC-53BP1 cells was decreased from 230±58 to 45±12 (P<0.05) and the protein expression of MMP-9 was significantly inhibited. However, the chemosensitivity of SKOV3/pLPC-53BP1 to cisplatin decreased significantly: Cisplatin half maximal inhibitory concentration (IC 50 ) for SKOV3/pLPC-53BP1=7.58±0.51 µg/ml; cisplatin IC 50 for control=2.98±0.27 µg/ml (P<0.01). Decreased chemosensitivity to cisplatin may be associated with increased expression of phosphorylated-protein kinase B and cyclin dependent kinase 2 and with decreased expression of p21 and the B cell lymphoma (Bcl)-2 associated X/Bcl-2 ratio. The results of the present study demonstrated that 53BP1 may inhibit migration but upregulate chemoresistance to cisplatin in SKOV3 cells.

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Overexpression of long non-coding RNA HOTAIR leads to chemoresistance by activating the Wnt/β-catenin pathway in human ovarian cancer

Cited by 178 publications

References 24 publications

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

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

Long Non-Coding RNAs: the New Horizon of Gene Regulation in Ovarian Cancer

53BP1 inhibits the migration and regulates the chemotherapy resistance of ovarian cancer cells

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