Atl

Li, Jie; Geng, Changran; Sun, Lu; Wang, Shujuan; Shen, Tian; Zheng, Guoyan; Fan, Wensheng; Yan, Zhengzheng; Yang, Yizhuo; You, Yanqin; Fu, Xiaoyu; Li, Lian; Huang, Ke; Li, Yali; Meng, Yuanguang

doi:10.1097/igc.0000000000000065

Cited by 20 publications

(11 citation statements)

References 30 publications

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“…One of the main genes predicted to be affected and to affect downstream gene expression was the DIRAS3 tumour suppressor. DIRAS3 is a GTPase belonging to the Ras superfamily and shares 50-60% homology with Ras and Rap, two other small GTP binding proteins, whose expression is reported to be reduced in 70% of invasive breast cancers (45,46) and 60% of ovarian cancers (47)(48)(49). DIRAS3 expression was markedly increased in PC3 miR-221del cells at gene and protein levels.…”

Section: Discussionmentioning

confidence: 99%

MiR-221 Is Specifically Elevated in PC3 Cells and its Deletion Reduces Adhesion, Motility and Growth

et al. 2019

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Background/Aim: MiR-221, often described both as an oncogenic microRNA and as a tumour suppressor, targets mRNAs involved in carcinogenesis. While other oncogenic microRNAs showed correlations with prostate cancer cell lines' aggressiveness, miR-221 showed an unusual overexpression in PC3. Materials and Methods: CRISPR was used to delete miR-221 from PC3 cells. Analysing the characteristics of PC3 miR-221del cells, a reduced growth rate and expression of cell-cycle genes was observed. In global gene expression/ontology analysis of PC3 miR-221del cells, cell-cell and cell-substrate adhesion pathways were found to be greatly affected. In addition, reduced levels of adhesion, invasion and motility for PC3 miR-221del cells, a change in F-actin localisation and a reduction of EMT markers were observed. Results: The tumour suppressor gene, DIRAS3, was a predicted target of miR-221. In PC3 miR-221del cells DIRAS3 was up-regulated at the gene and protein level. Ectopic expression of DIRAS3 in PC3 wt cells recapitulated the cellular morphology changes seen in PC3 miR-221del cells. DIRAS3 3'UTR was more stable in PC3 miR-221del cells, as measured by semi-quantitative PCR and luciferase fusion reporter assays. Conclusion: MiR-221 promotes aggressiveness of PC3 cells by down-regulating DIRAS3, and promoting epithelial-to-mesenchymal transition. 5311

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Section: Discussionmentioning

confidence: 99%

MiR-221 Is Specifically Elevated in PC3 Cells and its Deletion Reduces Adhesion, Motility and Growth

et al. 2019

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“…Altogether, these results indicated that the cilostazol protected myocardial I/R injury via activating TFEB, which was consistent with a previous study, although with distinct mechanism . It should be also mentioned that exaggerated autophagy may also promote heart failure development .Therefore, maintaining the hemostasis of autophagy is important for cardiac homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

Xiang

2019

Biotech and App Biochem

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Although cilostazol was proved to have antitumor biological effects, its function in myocardial ischemia and reperfusion (I/R) injury and the underlying mechanisms were not fully illustrated yet. In this study, a rat model of I/R injury was constructed and quantitative real-time PCR, Western blot, and immunofluorescence (IF) assay were performed. Our results showed that cilostazol increased LC3 II/LC3 I ratio, reduced p62 abundance, and promoted the expressions of LAMP1, LAMP2, cathepsin B, and cathepsin D, indicating that cilostazol could activate autophagy and elevated lysosome activation. Following analysis showed that cilostazol enhanced nuclear protein expression of transcription factor EB (TFEB), an important regulator of autophagy-lysosome pathway. Furthermore, CCI-779, an inhibitor of TFEB, could reverse the effects of cilostazol on autophagic activity and lysosome activation. Importantly, cilostazol suppressed I/R injury-induced apoptosis by decreasing the cleavage of caspase 3 and PARP. Enzyme-linked immunosorbent assay showed that cilostazol reduced the serum levels of CTn1 and CK-MB and decreased infract size caused by I/R injuries. Altogether this study suggested that cilostazol protects against I/R injury by regulating autophagy, lysosome, and apoptosis in a rat model of I/R injury. The protective mechanism of cilostazol was partially through increasing the transcriptional activity of TFEB.

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“…It has been reported that in HeLa cells, PI3K/AKT lies upstream of the Bcl-2 and can regulate its expression 35. Li et al found that ARHI can trigger PI3K/AKT pathway to modulate the expression of Bcl-2, and overexpressed ARHI could reduce the phosphorylation of AKT and increase the levels of PI3K inhibitor LY294002 to suppress the expression of Bcl-2 in epithelial ovarian cancer cells 36. This study found that overexpression of ARHI could reduce the protein expression of Bcl-2 to induce apoptosis in ECA109 cells.…”

Section: Discussionmentioning

confidence: 99%

The expression of <em>aplysia ras homolog I</em> (<em>ARHI</em>) and its inhibitory effect on cell biological behavior in esophageal squamous cell carcinoma

Mao

Shi

2017

OTT

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BackgroundAplysia ras homolog I (ARHI) is a Ras-related maternally imprinted tumor suppressor gene. Loss of ARHI expression contributes to the malignant progression of various tumors. However, reports on the clinical implications and functional role of ARHI expression in esophageal squamous cell carcinoma (ESCC) are limited. This study examined the role of ARHI in ESCC.MethodsIn total, 81 patients diagnosed with ESCC based on histopathological evaluations who were subjected to surgical resection were included in the study. ARHI expression was analyzed by immunohistochemistry and western blotting, examining the correlations between ARHI expression and patient clinicopathological features. The functional effects of ARHI overexpression were examined using a Cell Counting Kit-8 assay, flow cytometry, a Transwell assay, wound healing, and western blotting in the ECA109 cell line.ResultsARHI was highly expressed in 27.5% (22/81) of ESCC specimens (adjacent noncancerous tissues, 85.2%, 69/81; P<0.05). The ARHI expression level was significantly lower in patients with lymph node metastasis than in patients without (P<0.05). A Kaplan–Meier survival analysis showed that patients with low ARHI expression had shorter survival than patients with high expression (P<0.05), and a multivariate Cox analysis revealed that ARHI is an independent predictor of overall survival (P=0.029). Finally, overexpression of ARHI in ESCC cells indicates that ARHI suppresses proliferative capacity, invasive capacity, and cell cycle progression and may also suppress epithelial–mesenchymal transition and induce apoptosis and autophagy.ConclusionARHI may be a prognostic biomarker and a potential therapeutic target in ESCC.

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Atl

Cited by 20 publications

References 30 publications

MiR-221 Is Specifically Elevated in PC3 Cells and its Deletion Reduces Adhesion, Motility and Growth

MiR-221 Is Specifically Elevated in PC3 Cells and its Deletion Reduces Adhesion, Motility and Growth

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

The expression of <em>aplysia ras homolog I</em> (<em>ARHI</em>) and its inhibitory effect on cell biological behavior in esophageal squamous cell carcinoma

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