The role of miR-766-5p in cell migration and invasion in colorectal cancer

Jia, Bin; Lei, Xia; Cao, Fang

doi:10.3892/etm.2018.5716

Cited by 27 publications

(30 citation statements)

References 28 publications

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“…These data collectively suggest an antagonistic role of miR-766-5p and CASC15 on each other. A similar antagonistic role of miR-766-5p was observed by Jia et al in colorectal cancer where they showed that miR-766-5p inhibitor repressed the process of colorectal cancer by targeting suppressor of cancer cell invasion (SCAI) [26]. Wang et al found that miR-766 could serve as a novel p53 activator which functioned by targeting MDM4 and thereby enhancing the p53 signaling axis [27].…”

Section: Discussionsupporting

confidence: 58%

CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer

et al. 2019

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Long non-coding RNAs (lncRNAs) are key mediators of cancer. The dysregulation of a lncRNA, CASC15, has been linked to several cancers, except lung cancer. Here, the aim of the study was to explore the role and mechanism of CASC15 in lung cancer regulation, with the focus on its interaction with a potential target, microRNA-766-5p (miR-766-5p) and an oncogene, kallikreinrelated peptidase 12 (KLK12). Quantitative real-time PCR (qRT-PCR) was used to assess levels of CASC15, miR-766-5p and KLK12 in lung cancer tissues or cells. Western blot analysis was used to detect KLK12 protein expression. Ectopic expression of CASC15 was induced by a lentiviral system. CCK-8 and transwell assays were used to evaluate lung cancer cell proliferation and invasion, respectively. The interaction among CASC15, miR-766-5p and KLK12 was investigated by bioinformatical analysis and luciferase assay. In lung cancer tissue and cells, CASC15 was upregulated, while miR-766-5p was downregulated. Overexpression of CASC15 promoted lung cancer cell proliferation and invasion. A negative correlation was found between CASC15 and miR-766-5p levels. Overexpression of miR-766-6p reversed the cancer-promoting role of CASC15 in lung cancer cells, which was mediated by KLK12. The tumor-promoting role of CASC15 and tumorsuppressing role of miR-766-5p were also validated in vivo in tumor bearing mice, and KLK12 was also shown as an important mediator. CASC15 promotes lung cancer through the miR-766-5p/ KLK12 axis, indicating that CASC15 is a potential therapeutic in lung cancer.

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Section: Discussionsupporting

confidence: 58%

CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer

et al. 2019

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“…Jia et al found that miR-766 expression was increased in colorectal cancer and could function as an oncogene. 28 Similarly, Li et al demonstrated that miR-766 promoted cell proliferation of human colorectal cancer by inhibiting the expression of SOX6. 29 However, the expression status and biological function of miR-766 in OS are largely unknown.…”

Section: Discussionmentioning

confidence: 97%

<p>Circular RNA circ_0001105 Inhibits Progression and Metastasis of Osteosarcoma by Sponging miR-766 and Activating YTHDF2 Expression</p>

Yang¹,

Han²,

Li³

et al. 2020

OTT

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Background: Circular RNAs (circRNAs) play vital roles in the modulation of tumor progression. This study explored the biological functions of circ_0001105 in the progression of osteosarcoma (OS). Methods: qRT-PCR and in situ hybridization (ISH) were performed to detect the expression status of circ_0001105 in cells and tissues. Bioinformatics analysis, dual-luciferase reporter gene assay, Western blot and qRT-PCR were performed to determine the relationships among RNAs. The CCK-8, colony formation, EdU, transwell and wound healing assays were conducted to evaluate the cell growth, invasion and migration of OS cells. Tumor xenografts were established to investigate the effects of circ_0001105 on tumor growth in vivo. Lastly, the protein expression of YTHDF2 in OS tissues was measured using immunohistochemical staining. Results: Data showed that circ_0001105 and YTHDF2 were significantly lower, while miR-766 was higher in OS tissues compared to adjacent tissues. Low expression of circ_0001105 or YTHDF2 was associated with poor survival of OS patients as demonstrated by the Kaplan-Meier analysis. In addition, miR-766 was identified as a direct binding target of circ_0001105 and YTHDF2. Ectopic overexpression of circ_0001105 or YTHDF2 significantly suppressed OS cell viability and invasion through regulating miR-766. Last, overexpression of circ_0001105 significantly attenuated in vivo tumor growth. Conclusion: Our findings suggest that circ_0001105 inhibits OS progression, at least partially, by regulating miR-766/YTHDF2 signaling pathway.

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“…Wistar rats weighing 220-250 g and aged 10-12 weeks old were purchased from The Animal Centre of Nanchang University (Nanchang, China) and housed in our laboratory at 22-23˚C in 55-60% humidity, with a 12 h light/dark cycle, and free access to food and water. The rats underwent urinary bladder massage at least twice per day until the recovery of spontaneous micturition (9). The present study was approved by the Research Council and Animal Care and Use Committee of Shangrao People's Hospital (Shangrao, China), and performed according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals (9).…”

Section: Animals and Spinal Cord Surgery A Total Of 12 Malementioning

confidence: 99%

“…The rats underwent urinary bladder massage at least twice per day until the recovery of spontaneous micturition (9). The present study was approved by the Research Council and Animal Care and Use Committee of Shangrao People's Hospital (Shangrao, China), and performed according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals (9). Rats were randomly divided into two groups: Control (n=6) and SCI model (n=6).…”

Section: Animals and Spinal Cord Surgery A Total Of 12 Malementioning

confidence: 99%

miR‑34a alleviates spinal cord injury via TLR4 signaling by inhibiting HMGB‑1

Zhou

Shuang

et al. 2018

Exp Ther Med

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The aim of the present study was to investigate the effect of microRNA (miR)-34a on spinal cord injury (SCI)-induced inflammation and the possible underlying mechanisms. The results indicated that miR-34a expression was downregulated in a rat model of SCI compared with the control group. Furthermore, miR-34a knockdown was demonstrated to aggravate inflammation, inhibit cell proliferation and enhance apoptosis in an in vitro model of SCI. MiR-34a inhibition was demonstrated to upregulate the expression of inducible nitric oxide synthase and nitric oxide, as well as inducing the expression of toll-like receptor 4 (TLR4) and high mobility group box-1 (HMGB-1) in an in vitro model of SCI. TLR4 inhibitor reduced the effects of miR-34a downregulation on inflammation and cell growth in SCI. Together, these results suggest that miR-34a is able to alleviate SCI via inhibiting HMGB-1 expression in TLR4 signaling.

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The role of miR-766-5p in cell migration and invasion in colorectal cancer

Cited by 27 publications

References 28 publications

CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer

CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer

<p>Circular RNA circ_0001105 Inhibits Progression and Metastasis of Osteosarcoma by Sponging miR-766 and Activating YTHDF2 Expression</p>

miR‑34a alleviates spinal cord injury via TLR4 signaling by inhibiting HMGB‑1

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