Downregulation of long non‑coding RNA UCA1 enhances the radiosensitivity and inhibits migration via suppression of epithelial‑mesenchymal transition in colorectal cancer cells

Yang, Xiaodong; Liu, Wei; Xu, Xiaohui; Zhu, Jinming; Wu, Yong; Zhao, Kui; He, Songbin; Li, Ming; Wu, Yongyou; Zhang, Shuyu; Cao, Jianping; Ye, Zhenyu

doi:10.3892/or.2018.6573

Cited by 26 publications

(25 citation statements)

References 36 publications

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“…Moreover, incremental expression of CCAT1 and CCAT2 might enable aggressive growth and intrusion of CRC cells [13,14], and lncRNA MIR100HG was able to reinforce cetuximab-tolerance of CRC cells via activation of Wnt/βcatenin signaling [15]. With regard to lncRNA urothelial carcinoma associated 1 (UCA1), its high expression could reflect poor survival of CRC patients, and artificially raising its intracellular expression might powerfully enhance epithelial-mesenchymal transition (EMT) and radioresistance of CRC cells [16,17]. Apart from CRC, the oncogenic function of UCA1 was also embodied in nonsmall cell lung cancer [18], bladder cancer [19], breast cancer [20], tongue squamous cell carcinoma [21] and esophageal cancer [22], a portion of which were achieved through its interplay with specific miRNAs.…”

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confidence: 99%

SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression

Zhang

Cui

et al. 2020

Cell Commun Signal

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Background: This investigation was arranged to elucidate whether single nucleotide polymorphisms (SNPs) of lncRNA UCA1 was implicated in elevating colorectal cancer (CRC) risk by interacting with environmental exposures.Methods: LncRNASNP database was firstly adopted to predict SNPs that possibly affected binding of UCA1 with miRNAs and then the interactive effect of SNPs and environmental exposure on CRC risk was evaluated by recurring to type 2 gene-environment interactions (GEI) model. Besides, MTT assay, colony formation assay, transwell assay and wound healing assay were performed to assess the activity of CRC cell lines which carried distinct genotypes of specific SNPs. The impact of nicotine on activity of CRC cells was also appraised. Results: SNP rs12982687 of UCA1 intervened in the binding capacity of UCA1 with several miRNAs, especially miR-873-5p. MiRNAs regulated by UCA1, as predicted by mirPath software, shared genes that were enriched in HIF1 signaling pathway. Moreover, homozygote TT of rs12982687 reduced CRC risk among smokers, and CRC cells that carried rs12982687 (CC) displayed strong migration and invasion. By contrast, miR-873-5p mimic, which reduced UCA1 expression, delayed metastasis of CRC cells (all P < 0.05). Additionally, nicotine not merely elevated UCA1 and HIF-1α expressions in CRC cells, but also facilitated proliferation and metastasis of CRC cells (P < 0.05). Conclusions: SNP rs12982687 was involved in smoking-triggered CRC progression, given its influence on UCA1's binding with miR-873-5p and HIF-1 signaling.

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confidence: 99%

SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression

Zhang

Cui

et al. 2020

Cell Commun Signal

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“…Mechanistically, UCA1 promoted phosphorylation of several kinases implicated in tumor radioresistance and cell cycle regulation: AKT, FAK, FGR, and AMPKα1 [136]. Unlike in prostate cancer, UCA1 inhibition in CRC cells attenuated the G2/M arrest induced by IR, while it promoted apoptosis and inhibited migration and EMT of CRC cells [171]. Thus, the mechanism underlying UCA1 effect on radioresistance involves cell cycle regulation in prostate cancer, but apparently not in CRC.…”

Section: Lncrnasmentioning

confidence: 96%

Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

Podralska

Ciesielska

Kluiver

et al. 2020

Cancers

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Radiotherapy is a cancer treatment that applies high doses of ionizing radiation to induce cell death, mainly by triggering DNA double-strand breaks. The outcome of radiotherapy greatly depends on radiosensitivity of cancer cells, which is determined by multiple proteins and cellular processes. In this review, we summarize current knowledge on the role of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in determining the response to radiation. Non-coding RNAs modulate ionizing radiation response by targeting key signaling pathways, including DNA damage repair, apoptosis, glycolysis, cell cycle arrest, and autophagy. Additionally, we indicate miRNAs and lncRNAs that upon overexpression or inhibition alter cellular radiosensitivity. Current data indicate the potential of using specific non-coding RNAs as modulators of cellular radiosensitivity to improve outcome of radiotherapy.

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“…What's more, lncRNA UCA1 is upregulated in CRC and induces therapy resistance. Suppression of UCA1 decreases colony formation, proliferation, and EMT, at the same time, triggers apoptosis and G2-M arrest [74]. In addition, HOTAIR is also related to the regulation of apoptosis after radiotherapy, showing that it can be used as a potential therapeutic target [75].…”

Section: Colorectal Cancer (Crc)mentioning

confidence: 99%

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

et al. 2020

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As the standard treatments for cancer, chemotherapy and radiotherapy have been widely applied to clinical practice worldwide. However, the resistance to cancer therapies is a major challenge in clinics and scientific research, resulting in tumor recurrence and metastasis. The mechanisms of therapy resistance are complicated and result from multiple factors. Among them, non-coding RNAs (ncRNAs), along with their modifiers, have been investigated to play key roles in regulating tumor development and mediating therapy resistance within various cancers, such as hepatocellular carcinoma, breast cancer, lung cancer, gastric cancer, etc. In this review, we attempt to elucidate the mechanisms underlying ncRNA/modifier-modulated resistance to chemotherapy and radiotherapy, providing some therapeutic potential points for future cancer treatment.

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Downregulation of long non‑coding RNA UCA1 enhances the radiosensitivity and inhibits migration via suppression of epithelial‑mesenchymal transition in colorectal cancer cells

Cited by 26 publications

References 36 publications

SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression

SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression

Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

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