miR‐374a promotes cell proliferation, migration and invasion by targeting SRCIN1 in gastric cancer

Xu, Xinyun; Wang, Weijun; Su, Ning; Zhu, Xiongzhao; Yao, Jun; Gao, Wenchao; Hu, Zhiqian; Sun, Yanping

doi:10.1016/j.febslet.2014.12.027

Cited by 70 publications

(59 citation statements)

References 31 publications

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“…Unlike previous reports in other cancers [7, 8], we showed miR-374a considerably inhibits proliferation, invasion and migration both in vitro and in vivo . We found that miR-374a inactives PI3K/AKT pathway by directly reducing CCND1, a link not previously published to our knowledge.…”

Section: Introductioncontrasting

confidence: 99%

“…miR-374a, located on chromosome Xq13.2, promotes or suppresses development of human cancer according to different studies. Some reports identified that miR-374a triggers epithelial-mesenchymal transition (EMT) in breast cancer and promotes cell proliferation in gastric cancer [7, 8], while Võsa et al found low expression of miR-374a in early-stage NSCLC is correlated with poorer patient survival [9]. In colorectal cancer, Slattery et al found that hsa-miR-374a-5p significantly reduces mortality for all 1141 CRC cases examined [10].…”

Section: Introductionmentioning

confidence: 99%

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microRNA-374a suppresses colon cancer progression by directly reducing CCND1 to inactivate the PI3K/AKT pathway

et al. 2016

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microRNA-374a (miR-374a) exhibits oncogenic functions in various tumor types. Here we report that miR-374a suppresses proliferation, invasion, migration and intrahepatic metastasis in colon adenocarcinoma cell lines HCT116 and SW620. Notably, we detected that PI3K/AKT signaling and its downstream cell cycle factors including c-Myc, cyclin D1 (CCND1), CDK4 and epithelial-mesenchymal transition (EMT)-related genes including ZEB1, N-cadherin, Vimentin, Slug, and Snail were all significantly downregulated after miR-374a overexpression. Conversely, cell cycle inhibitors p21 and p27 were upregulated. Expression of E-cadherin was only decreased in HCT116, without any obvious differences observed in SW620 cells. Furthermore, luciferase reporter assays confirmed that miR-374a could directly reduce CCND1. Interestingly, when CCND1 was silenced or overexpressed, levels of pPI3K, pAkt as well as cell cycle and EMT genes were respectively downregulated or upregulated. We examined miR-374a levels by in situ hybridization and its correlation with CCND1 expression in CRC tumor tissues. High miR-374a expression with low level of CCND1 was protective factor in CRC. Together these findings indicate that miR-374a inactivates the PI3K/AKT axis by inhibiting CCND1, suppressing of colon cancer progression.

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Section: Introductioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

microRNA-374a suppresses colon cancer progression by directly reducing CCND1 to inactivate the PI3K/AKT pathway

et al. 2016

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“…In addition, forced expression of miR-153 suppressed the migration and invasion capacity of GC cell lines and vice versa, indicating that miR-153 functions as a tumor suppressor in GC. Xu et al (2015) reported that miR-374a was overexpressed in human GC cell lines and tissues. Inhibition of miR-374a was able to suppress GC cell proliferation, migration, and invasion in vitro and retarded tumor growth in vivo, suggesting that miR-374a may promote the tumorigenesis of GC.…”

Section: Introductionmentioning

confidence: 99%

Reduced expression of serum miR-204 predicts poor prognosis of gastric cancer

Chen

Liu

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Deregulation of microRNAs (miRNAs) is implicated in the initiation and progression of gastric cancer (GC). Previous studies have demonstrated that miR-204 was downregulated in GC tissues. However, its expression profile in serum samples and its potential for clinical value remain unknown. Real-time PCR was performed to evaluate the expression level of serum miR-204 in patients with GC. The association between serum miR-204 expression level and the clinical outcome of GC was then investigated. Our results showed that the expression of miR-204 in serum samples from GC patients was significantly lower than that in the healthy controls (P < 0.01). Serum miR-204 expression level of GC patients was significantly upregulated after receiving surgical resection (P < 0.01). In addition, serum miR-204 was associated with lymph node metastasis (P = 0.016), tumor differentiation (P = 0.001), and TNM stage (P = 0.005). GC patients with low serum miR-204 expression had shorter overall survival than those with high serum miR-204 expression (P = 0.004). Multivariate analysis revealed that serum miR-204 expression level was an independent risk factor for this malignant disease (HR = 3.629, 95%CI = 2.828-8.146, P = 0.015). In conclusion, our findings indicate that serum miR-204 may be employed as a novel biomarker for monitoring the treatment response and predicting the prognosis of GC.

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“…Additionally, the enforced expression of miR-211 could significantly reduce SRCIN1 protein expression in NSCLC cells. SRCIN1 contains two proline-rich regions, two coiled-coil domains and two regions containing highly charged amino acids [39,40]. A previous study showed a positive interaction between SRCIN1 expression and breast cancer; SRCIN1 was shown to inhibit the spreading, migration, and invasion of breast cancer cells [41].…”

Section: Discussionmentioning

confidence: 99%

miR-211 promotes non-small cell lung cancer proliferation by targeting SRCIN1

Wang

Liu

2015

Tumor Biol.

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MicroRNAs (miRNAs) are a class of small non-coding RNAs that, when dysregulated, are involved in the initiation and progression of various cancers, including lung cancer, in humans. In the current study, qRT-PCR was performed to measure miR-211 expression in human non-small cell lung cancer (NSCLC) cell lines and tissues. Cell proliferation, cell cycle, colony formation, and invasion were performed to detect the functional role of miR-211 in human NSCLC cell line. We used luciferase reporter assay to find the potential target of miR-211. We found that miR-211 expression was upregulated in human non-small cell lung cancer (NSCLC) cell lines and tissues. The overexpression of miR-211 enhanced NSCLC cell proliferation, colony formation, and invasion. SRC kinase signaling inhibitor 1 (SRCIN1) was identified as a direct target of miR-211. SRCIN1 silencing promoted cell proliferation, and SRCIN1 expression was downregulated in human NSCLC cell lines. Thus, miR-211 may function as an oncogenic miRNA in NSCLC, partly by regulating SRCIN1, and the modulation of miR-211 expression represents a potential strategy for the treatment of NSCLC patients.

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miR‐374a promotes cell proliferation, migration and invasion by targeting SRCIN1 in gastric cancer

Cited by 70 publications

References 31 publications

microRNA-374a suppresses colon cancer progression by directly reducing CCND1 to inactivate the PI3K/AKT pathway

microRNA-374a suppresses colon cancer progression by directly reducing CCND1 to inactivate the PI3K/AKT pathway

Reduced expression of serum miR-204 predicts poor prognosis of gastric cancer

miR-211 promotes non-small cell lung cancer proliferation by targeting SRCIN1

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