Regulation of the P2X7R by microRNA-216b in human breast cancer

Zheng, Luming; Zhang, Xukui; Yang, Feng; Zhu, Jian; Zhou, Peng; Yu, Fang; Hou, Lei; Xiao, Lei; He, Qingqing; Wang, Baocheng

doi:10.1016/j.bbrc.2014.07.101

Cited by 53 publications

(31 citation statements)

References 23 publications

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“…In addition, miR-216b was demonstrated to be underexpressed in breast cancer. The ectopic expression of miR-216 targeted purinergic receptor P2X 7 and decreased the level of growth of breast cancer cells (33). Additional studies revealed that nasopharyngeal carcinoma cells exhibited lower miR-216b expression and inhibited proliferation, migration and invasion by targeting V-Ki-ras2 Kirsten rate sarcoma viral oncogene and protein kinase C α (34,35).…”

Section: Discussionmentioning

confidence: 98%

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

et al. 2018

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Abstract. Micro (mi)RNAs are small, evolutionarily conserved and endogenous noncoding RNA molecules between 19 and 24 nucleotides in length. The potential roles of miRNAs in the carcinogenesis and progression of non-small cell lung cancer (NSCLC) have been studied previously. In the present study, it was revealed that miRNA-216b (miR-216b) expression was lower in NSCLC tissue and cell lines compared with that in adjacent healthy lung tissue samples and the normal bronchial epithelial 16HBE cell line, respectively. The ectopic expression of miR-216b inhibited the proliferation and invasion of NSCLC cells in vitro. SRY-Box 9 (SOX9) was identified as a direct target of miR-216b in NSCLC. In addition, SOX9 small interfering RNA was able to mimic the effects of miR-216b overexpression on cell proliferation and invasion in NSCLC. Therefore, the data reported in the present study demonstrate that miR-216b is an important tumor suppressor in NSCLC. These data may contribute to the understanding of the molecular mechanism underlying the carcinogenesis and progression of NSCLC, and provide novel therapies for patients with NSCLC.

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Section: Discussionmentioning

confidence: 98%

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

et al. 2018

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“…Significant existing literature has provided verification indicating the involvement of lncRNAs in cancer biology, with lncRNAs exhibiting stimulated levels in a variety of malignancies, highlighting their usefulness as biomarkers and therapeutic targets. 10,22,23 Thus, the present study aimed to explore the effects of the novel lncRNA LINC01305 on the cell invasion, migration and EMT of CC [25][26][27][28] Existing literature has revealed that lncRNAs play a role in CC through the regulation of various signalling pathways. ANRIL has been correlated with poor CC prognoses and play crucial roles in the process of tumourigenesis through activation of the PI3K-Akt signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

Yan

Chu

Qiu

et al. 2019

J Cellular Molecular Medi

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Cervical cancer (CC) remains one of the leading malignancies afflicting females worldwide, with its aetiology associated with long‐term papillomavirus infection. Recent studies have shifted their focus and research attention to the relationship between long non‐coding RNAs (lncRNAs) and CC therapeutic. Thus, the aim of the current study was to investigate the underlying mechanism of lncRNA LINC01305 on the cell invasion, migration and epithelial‐mesenchymal transition (EMT) of CC cells via modulation of the PI3K/Akt signalling pathway by targeting tenascin‐X B (TNXB). The expressions of LINC01305, TNXB, MMP2, MMP9, E‐cadherin, vimentin, PI3K, Akt, p‐PI3K, p‐Akt and TNXB were detected in this study. After which, the cell invasion and migration abilities of the CC cells were determined respectively. Bioinformatics and the application of a dual luciferase reporter gene assay provided verification indicating that TNXB is the target gene of lncRNA LINC01305. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis methods revealed that the expressions of MMP2, MMP9, vimentin, PI3K, Akt, p‐PI3K and p‐Akt were decreased following the down‐regulation of LncRNA LINC01305 or overexpression of TNXB. LncRNA LINC01305 silencing or TNXB overexpression was noted to decrease the migration and invasion of SiHa cells. Taken together, the key findings of the current study present evidence suggesting that lncRNA LINC01305 silencing suppresses EMT, invasion and migration via repressing the PI3K/Akt signalling pathway by means of targeting TNXB in CC cells, which ultimately provides novel insight and identification of potential therapeutic targets for CC.

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“…A previous study revealed that the ectopic expression of miR-216b decreased the proliferation, migration and invasion of hepatocellular carcinoma cells by targeting insulin like growth factor 2 mRNA binding protein 2 (29). Zheng et al (30) demonstrated that miR-216b was downregulated in breast cancer, and targeted P2X purinoceptor 7 to attenuate cell growth and enhance apoptosis. Deng et al (32,33) indicated that miR-216b suppressed nasopharyngeal carcinoma cell proliferation and invasion via blockade of K-Ras and protein kinase Cα.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑216b reduces growth, migration and invasion of pancreatic ductal adenocarcinoma cells by directly targeting ρ‑associated coiled‑coil containing protein kinase 1

et al. 2018

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Abstract. Developments in cancer therapy have greatly improved the survival time for patients with pancreatic ductal adenocarcinoma (PDAC); however, the prognosis of patients with PDAC remains poor. Understanding the expression patterns and functions of microRNAs may provide strategies for the diagnosis and treatment of patients with PDAC. The present study aimed to explore the expression and functions of microRNA-216b (miR-216b) in PDAC. The expression of miR-216b in PDAC tissues and cell lines was quantified with reverse transcription-quantitative polymerase chain reaction. An miR-216b mimic was introduced into PDAC cells to induce the effects of miR-21b overexpression. The effects of miR-216b overexpression on growth, migration and invasion of PDAC cells were evaluated by cell proliferation assay, migration and invasion assays, respectively. The molecular mechanism underlying the suppressive effects of miR-216b on PDAC was also examined; a direct target gene of miR-216b, ρ-associated coiled-coil containing protein kinase 1 (ROCK1), was downregulated by ROCK1 short interfering RNA to investigate the effects on growth, migration and invasion of PDAC cells. The present study revealed that miR-216b was significantly downregulated in PDAC tissues and cell lines. Overexpression of miR-216b inhibited growth, migration and invasion of PDAC cells in vitro. ROCK1 was identified as a direct target gene of miR-216b in pancreatic cancer and the downregulation of ROCK1 resembled the effects of miR-216b overexpression in PDAC cells. Taken together, miR-216b acted as a tumor suppressor in PDAC and may represent a novel therapeutic target in PDAC.

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Regulation of the P2X7R by microRNA-216b in human breast cancer

Cited by 53 publications

References 23 publications

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

MicroRNA‑216b reduces growth, migration and invasion of pancreatic ductal adenocarcinoma cells by directly targeting ρ‑associated coiled‑coil containing protein kinase 1

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