Screening of differential microRNA expression in gastric signet ring cell carcinoma and gastric adenocarcinoma and target gene prediction

Chen, Jian; Sun, Di; Chu, Hongjin; Gong, Zhaohui; Zhang, Chenglin; Gong, Benjiao; Li, Yan; Li, Ning; Jiang, Lixin

doi:10.3892/or.2015.3935

Cited by 41 publications

(36 citation statements)

References 63 publications

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“…24 It is reported that IBD has the risk of developing colitis associated cancer (CAC), and the increasing cancer incidence has been up to 20%. 25 Polytarchou et al .…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR-665 promotes apoptosis and colitis in inflammatory bowel disease by repressing the endoplasmic reticulum stress components XBP1 and ORMDL3

Zhang

Qiu

et al. 2017

Cell Death Dis

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MicroRNAs are critical post-transcriptional regulators of gene expression and key mediators of pathophysiology of inflammatory bowel disease (IBD). This study is aimed to study the role of miR-665 in the progression of IBD. Real-time PCR analysis was used to determine miR-665 expression in 89 freshly isolated IBD samples and dextran sulfate sodium (DSS)-induced colonic mucosal tissues. The role of miR-665 in inducing apoptosis and colitis were examined by Annexin V, TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining, colony formation in vitro and DSS-induced colitis mice model in vivo. Moreover, luciferase reporter assay, western blot analysis and microribonucleoprotein immunoprecipitation were performed to determine that miR-665 directly repressed XBP1 (X-box-binding protein-1) and ORMDL3 expression. Herein, our results revealed that miR-665 was markedly upregulated in active colitis. Gain-of-function and loss-of-function studies showed that ectopic expression of miR-665 promoted apoptosis under different inflammatory stimuli. Importantly, delivery of miR-665 mimic promoted, while injection of antagomiR-665 markedly impaired DSS-induced colitis in vivo. Mechanistically, we demonstrated that miR-665 induced apoptosis by inhibiting XBP1 and ORMDL3. Taken together, our findings reveal a new regulatory mechanism for ER stress signaling and suggest that miR-665 might be a potential target in IBD therapy.

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“…24 It is reported that IBD has the risk of developing colitis associated cancer (CAC), and the increasing cancer incidence has been up to 20%. 25 Polytarchou et al .…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR-665 promotes apoptosis and colitis in inflammatory bowel disease by repressing the endoplasmic reticulum stress components XBP1 and ORMDL3

Zhang

Qiu

et al. 2017

Cell Death Dis

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“…The impact of specific miRNAs on cancer biology depends on their downstream targets [49, 50]. Different prediction algorithms were used to predict gene targets for miR-124 so that to elucidate the underlying mechanisms involved in the miR-124-induced inhibition of bladder cancer growth invasion and migration.…”

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

Xiong

Wang

et al. 2017

Cell Physiol Biochem

102

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Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

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“…In our study, the real-time PCR results indicated that miR-140's expression level was obviously downregulated in both PDAC tissues and cell lines. Manually enhanced expression of Since the effect of certain miRNAs on carcinogenesis depends on their downstream targets [24,25], various predictive algorithms were used to calculate target sequences for miR-140 in order to clarify the corresponding reaction chains involved in the inhibition of PDAC's proliferation and metastasis by induction of miR-140. The iASPP oncogene was verified as an important downstream target of miR-140 because of its frequent overexpression in many types of cancer and serves as an essential modulator of cell replication, survival, and migration [26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-140 regulates cell growth and invasion in pancreatic duct adenocarcinoma by targeting iASPP

Liang

Gong

Zhang

et al. 2016

ABBS

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MicroRNAs are ∼22 nucleotide RNAs processed from RNA hairpin structures that play important roles in regulating protein expression level via binding to mRNA, either suppressing its translation or speeding up its degradation. In humans, they regulate most protein-coding genes, including genes important in cancer and other diseases. In this study, the expression of microRNA-140 (miR-140) was demonstrated to be significantly suppressed in pancreatic duct adenocarcinoma specimens and cell lines, compared with their adjacent normal tissues. With the help of bioinformatics analysis, inhibitor of apoptosis-stimulating protein of p53 (iASPP) was identified to be a direct target of miR-140, and luciferase reporter experiment confirmed this discovery. Overexpression of miR-140 decreases the protein expressions of iASPP, ΔNp63, MMP2, and MMP9. Growth and invasion of PANC-1 cells were attenuated by overexpression of miR-140 in vitro. The suppressive effect of miR-140 on PANC-1 cell line could be partly balanced out by manual overexpression of iASPP. Above all, these findings provided insights into the functional mechanism of miR-140, suggested that the miR-140/iASPP axis may interfere with the proliferative and invasive property of pancreatic duct adenocarcinoma cells, and indicated that miR-140 could be a potential therapeutic target for pancreatic duct adenocarcinoma.

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Screening of differential microRNA expression in gastric signet ring cell carcinoma and gastric adenocarcinoma and target gene prediction

Cited by 41 publications

References 63 publications

Upregulation of miR-665 promotes apoptosis and colitis in inflammatory bowel disease by repressing the endoplasmic reticulum stress components XBP1 and ORMDL3

Upregulation of miR-665 promotes apoptosis and colitis in inflammatory bowel disease by repressing the endoplasmic reticulum stress components XBP1 and ORMDL3

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

MicroRNA-140 regulates cell growth and invasion in pancreatic duct adenocarcinoma by targeting iASPP

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