miR-128 and its target genes in tumorigenesis and metastasis

Li, Molin; Fu, Weiming; Wo, Lulu; Shu, Xiaohong; Liu, Fang; Li, Chuangang

doi:10.1016/j.yexcr.2013.07.031

Cited by 96 publications

(80 citation statements)

References 62 publications

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“…miR-128 specifically inhibits a number of target genes related to tumor cell characteristics, including apoptosis and proliferation (8,9). Evidence suggests that miR-128 is an apoptosis-induced factor and functions at least in part by targeting a host of apoptosis-related genes, including Bmi-1, EGFR and E2F3 (10). miR-128 may silence the expression of certain anti-apoptotic genes and induce apoptosis in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

et al. 2015

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Abstract. In this study, we investigate whether miR-128 is capable of regulating the apoptosis and proliferation of human U251 glioma cells by downregulating RhoE. The expression of miR-128 was assessed by quantitative polymerase chain reaction in normal brain tissue and glioma samples. A significant downregulation of the expression of miR-128 was detected in glioma in contrast to normal brain tissue. Following the transfection of pre-miR-128 and anti-miR-128 into U251 cells, the high expression of miR-128 could inhibit proliferation and induce apoptosis in U251 cells, and those effects could be restored by miR-128 knockdown. To analyze the regulation mechanism of miR-128, TargetScan, miRanda and PicTar were used to ascertain whether RhoE was a potential target gene. Next, luciferase activity assay and western blot analysis confirmed that RhoE was a direct and specific target gene of miR-128. The advanced effects of pre-miR-128 on the apoptosis and proliferation of U251 cells were reversed by the upregulation of RhoE expression. In summary, aberrantly expressed miR-128 regulates apoptosis and proliferation in human glioma U251 cells partly by directly targeting RhoE. This finding may offer a new potential therapeutic strategy for the treatment of glioma.

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Section: Introductionmentioning

confidence: 99%

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

et al. 2015

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“…These findings suggested that miR-128b had an important role on inhibiting the development and progression of GC. MiR-128 is a kind of intronic miRNAs and encoded by two distinct genes, miR-128-1 and miR-128-2, which are located on human chromosome 2q21.3 and 3p22.3 respectively (Li et al 2013). Volinia found that the expression of miR-128b was significantly up-regulated in tumour tissues of colon, lung and pancreas comparing with normal tissues (Volinia et al 2006).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNA-128 (miR-128) is brain-enriched, including miR-128a and miR-128b (Li et al 2013). Aberrant expression of miR-128 is observed in many malignant tumours; however, the role of miR-128 in individual tumours is different.…”

Section: Introductionmentioning

confidence: 99%

MiR-128b is down-regulated in gastric cancer and negatively regulates tumour cell viability by targeting PDK1/Akt/NF-κB axis

et al. 2016

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Gastric cancer (GC) is the fourth most prevalent type of cancer worldwide, which is usually caused by the interaction between environmental and genetic factors, or epigenetic aspects. Referring to the non-coding RNAs, miR-128b has been reported to be associated with many tumour cases, and exerts distinct functions in different types of cancers. However, the function of miR-128b in GC onset and progression largely remains unknown. In the present study, we found that miR-128b expression was down-regulated in tissues from 18 GC patients and 3 carcinoma cell lines. In turn, over-expression of miR-128b suppressed GC cell proliferation, invasion and promoted apoptosis. Moreover, miR-128b was predicted to bind the 3'UTR of PDK1 gene using bioinformatic target-screening tools. Accordingly, ectopic expression of miR-128b inhibited the PDK1 expression at both transcriptional and post-transcriptional levels, and furthermore, the expression of gene tailed by the 3'UTR of PDK1 gene was significantly decreased in a dualluciferase reporter assay, suggesting that PDK1 was a direct target of miR-128b in GC cells. In the conditon of miR- 128b over-expression, we also observed spontaneous inactivation of the Akt/NF-κB signalling, implying PDK1 was a potential regulator of this pathway. In conclusion, our study shed some novel light on miR-128b-PDK1/Akt/NF-κB axis on GC progression.

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“…Clinical evidence suggested that H. pylori is related to gastric cancer, but the mechanism remained unclear [12]. Majority of cancer-related death is caused by metastasis and recent studies have demonstrated that miRNAs play an important role in the regulation of metastasis process [13]. However, their association with gastric cancer remains largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of miR-141 Induced by Helicobacter Pylori Promotes the Invasion of Gastric Cancer by Targeting STAT4

Zhou

Xia²,

Su³

et al. 2014

Cell Physiol Biochem

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Background: The association between Helicobacter pylori infection and gastric cancer has been identified recently. However, the molecular mechanism remained largely unknown. Methods and Results: We found that miR-141 was decreased in Helicobacter pylori positive specimens (n=75) compared with negative tissues (n=75). The knockdown of miR-141 enhanced the invasion ability of gastric cancer cells; meanwhile, over-expression of miR-141 could inhibit the abilities of gastric cancer cells in vitro. A luciferase assay revealed that miR-141 was directly bound to the 3'-untranslated regions (3'-UTR) of STAT4. STAT4 was found up-regulated at mRNA and protein levels, as shown by qRT-PCR and western blot. Over-expression of STAT4 was used to mimic miR-141 action in the invasion of gastric cancer. Conclusion: MiR-141 may play a pivotal role in controlling gastric cancer invasion through regulating STAT4 and maybe a potential target to treat gastric cancer.

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miR-128 and its target genes in tumorigenesis and metastasis

Cited by 96 publications

References 62 publications

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

MiR-128b is down-regulated in gastric cancer and negatively regulates tumour cell viability by targeting PDK1/Akt/NF-κB axis

Down-Regulation of miR-141 Induced by Helicobacter Pylori Promotes the Invasion of Gastric Cancer by Targeting STAT4

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