&lt;p&gt;miR-625 reverses multidrug resistance in gastric cancer cells by directly targeting ALDH1A1&lt;/p&gt;

Gong, Xufei; Xu, Bo; Li, Zi; Chen, Xinrui

doi:10.2147/cmar.s208708

Cited by 22 publications

(20 citation statements)

References 40 publications

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“…HMGA2 involvement in EMT is very well documented in a variety of tumors, and we have discussed some of its involvement in tumor EMT and migration in connection with NCCs [146,147,[150][151][152][153][154][211][212][213][214][215][216][217][218][219]. HMGA2 is also involved in EMT of crystalline epithelial cells in lens fibrosis; this process apparently uses the same pathway of TGFβ-regulated EMT, recruiting SMAD3, HMGA2, and SNAI [220][221][222].…”

Section: Hmga In Emtmentioning

confidence: 98%

HMGA Genes and Proteins in Development and Evolution

Vignali

Marracci

2020

IJMS

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HMGA (high mobility group A) (HMGA1 and HMGA2) are small non-histone proteins that can bind DNA and modify chromatin state, thus modulating the accessibility of regulatory factors to the DNA and contributing to the overall panorama of gene expression tuning. In general, they are abundantly expressed during embryogenesis, but are downregulated in the adult differentiated tissues. In the present review, we summarize some aspects of their role during development, also dealing with relevant studies that have shed light on their functioning in cell biology and with emerging possible involvement of HMGA1 and HMGA2 in evolutionary biology.

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Section: Hmga In Emtmentioning

confidence: 98%

HMGA Genes and Proteins in Development and Evolution

Vignali

Marracci

2020

IJMS

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“…Thus, miRNAs are thought to be markers of cancers diagnosis, progression, and prognosis . Many human miRNAs have been confirmed to be dysregulated in GC, including miR‐32‐5p, miR‐544a, miR‐1297, miR‐625, and miR‐383‐5p . Up to now, miR‐665 has been reported to function as an oncogene in breast cancer, hepatocellular carcinoma, acute lymphoblastic leukaemia, or function as a tumour suppressor in colorectal cancer, cervical cancer, and ovarian cancer; the functions of miR‐665 in GC were rare unexplored previously.…”

Section: Introductionmentioning

confidence: 99%

microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

Zhang¹,

Wang

Yi³

et al. 2020

Cell Biochemistry & Function

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Recently, microRNA-665 (miR-665) has been reported to function as both tumour suppressor and oncogene in several cancer types, including gastric cancer, hepatocellular cancer, and lung cancer. However, the biological function of miR-665 and its precise mechanisms in gastric cancer (GC) have not been well clarified. The aim of this study was to study the roles of miR-665/PPP2R2A axis in GC. The levels of PPP2R2A and miR-665 were detected by quantitative PCR assay in GC tissues and cell lines. Moreover, the biological roles of miR-665 and PPP2R2A in GC cells were assessed by cell proliferation, invasion, and epithelial-mesenchymal transition (EMT).The mRNA and protein levels of PPP2R2A were determined by using quantitative PCR and Western blotting assays. Luciferase assays were used to confirm that PPP2R2A was one target of miR-665. In this study, the miR-665 level was dramatically reduced in GC tissues and cell lines, and the PPP2R2A expression was significantly enhanced. What is more, the PPP2R2A expression was negatively related to the miR-665 level in GC tissues. Furthermore, up-regulation of miR-665 obviously restrained GC cells proliferation, invasion, and EMT. We confirmed that miR-665 could directly target PPP2R2A by luciferase reporter assay. Besides, knockdown of PPP2R2A also could markedly inhibit the proliferation, invasion and EMT of GC cells.Finally, overexpression of miR-665 in GC cells partially reversed the promoted effects of PPP2R2A up-regulation. Overexpression of miR-665 restrained GC cells proliferation, invasion and EMT via regulation of PPP2R2A.Significance of the study miR-665 has been reported to function as oncogene or tumour suppressor in different cancers. However, the precise roles of miR-665 in GC have not been elucidated. Our study for the first time demonstrated that miR-665 level was significantly down-regulated in GC. Additionally, miR-665 overexpression inhibited cell growth, invasion, and EMT of GC. Moreover, our data suggested a significant negative correlation between miR-665 and PPP2R2A expression in GC. MiR-665 suppressed GC cell proliferation, invasion, and EMT by directly targeting PPP2R2A, which suggested important roles for miR-665/PPP2R2A axis in the GC pathogenesis and its potential application in cancer therapy.

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“…Noticeably, miRNAs are strongly implicated in the chemotherapy resistance of GC. For example, Gong et al (17) found that the expression of miR-625 was decreased in multidrug resistance compared to that of the chemosensitive counterparts, and overexpression of miR-625 significantly enhanced the sensitivity and induced cell apoptosis in GC. Li et al (18) demonstrated that miR-200c-3p upregulation reversed drug resistance of human GC via regulating NER-ERCC3/ 4 pathway.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-4290 suppresses PDK1-mediated glycolysis to enhance the sensitivity of gastric cancer cell to cisplatin

Qian

Wang

et al. 2020

Braz J Med Biol Res

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The development of chemotherapy resistance significantly impairs the efficiency of chemotherapy, but the underlying mechanisms of chemotherapy resistance in gastric cancer (GC) are complicated and still need to be further explored. Here, we aimed to reveal the effects of miR-4290/PDK1 (pyruvate dehydrogenase kinase 1) axis on chemotherapy resistance of GC in vitro. The expression patterns of miR-4290 in GC tissues and cell lines were determined by real-time quantitative PCR. Kaplan-Meier was used to assess the relationship between miR-4290 expression levels and patients' overall survival. CCK-8 and flow cytometry technologies were applied to detect cell proliferation and apoptosis. The luciferase gene reporter assay was used to evaluate the interaction between miR-4290 and PDK1. miR-4290 was lowly expressed in GC tissues and cell lines, which was closely associated with the shorter overall survival of GC patients. miR-4290 mimics significantly inhibited cell proliferation and induced cell apoptosis, as well as induced a significant reduction in the expression of PDK1. Moreover, miR-4290 significantly inhibited glycolysis and decreased the IC50 value to cisplatin in SGC7901 cells, whereas these effects were abolished and cell apoptosis was promoted when PDK1 was overexpressed. In conclusion, this study revealed that miR-4290 suppressed PDK1-mediated glycolysis to enhance the sensitivity of GC cells to cisplatin.

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<p>miR-625 reverses multidrug resistance in gastric cancer cells by directly targeting ALDH1A1</p>

Cited by 22 publications

References 40 publications

HMGA Genes and Proteins in Development and Evolution

HMGA Genes and Proteins in Development and Evolution

microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

MicroRNA-4290 suppresses PDK1-mediated glycolysis to enhance the sensitivity of gastric cancer cell to cisplatin

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