miR-505-5p and miR-193b-3p: potential biomarkers of imatinib response in patients with chronic myeloid leukemia

Ramachandran, Suganthi S.; Muiwo, Pamchui; Pandey, Ravindra Mohan; Singh, Surender; Bakhshi, Sameer; Kumar, Lalit; Bhattacharya, Alok; Gupta, Yogendra Kumar

doi:10.1080/10428194.2016.1272681

Cited by 13 publications

(7 citation statements)

References 15 publications

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“…In addition, miRanda database analysis reveals that miR-505, which suppresses cell proliferation in hematological malignancies, is the potential target of lnc-MVIH (15,16,22). Then we detected the expression of miR-505 after transfecting lnc-MVIH shRNA into KG-1 cells and found that lnc-MVIH knockdown upregulated the expression of miR-505.…”

Section: Discussionmentioning

confidence: 96%

“…In our study, we observed that lnc-MVIH was overexpressed in AML cell lines compared with primary normal BMMC, and lnc-MVIH knockdown inhibited cell proliferation but promoted cell apoptosis in AML. The possible reasons might include that (I) lnc-MVIH might serve as the sponge for miRNA (such as miR-505 ), leading to the inhibitory effect on miRNA target genes (such as HMGB1 and CCNE2 ), contributing to the AML progression ( 16 ). (II) Lnc-MVIH knockdown might inactivate the oncogenic pathways such as WNT signaling pathway to inhibit the malignant progression ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

“…However, little is known about its role in hematological malignancies. In addition, lnc-MVIH contains target sites for miR-505 as retrieved from miRanda database analysis ( www.miranda.org ), which is a tumor suppressor in several malignancies including chronic myeloid leukemia ( 14 - 16 ). Therefore, we hypothesized that lnc-MVIH might interact with miR-505 as well as miR-505 downstream target genes and regulate AML progression.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA MVIH knockdown inhibits the malignancy progression through downregulating miR-505 mediated HMGB1 and CCNE2 in acute myeloid leukemia

Ke¹,

Zhou²

2019

Transl. Cancer Res.

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Background: This study aimed to investigate the regulatory role of long non-coding RNA associated with microvascular invasion in hepatocellular carcinoma (lnc-MVIH) in the progression of acute myeloid leukemia (AML) and the underlying mechanism. Methods: Lnc-MVIH expression was detected in AML cell lines AML-193, KG-1, HL-60, OCI-AML2 and primary normal bone marrow mononuclear cells (BMMC). The effect of lnc-MVIH knockdown on cell proliferation, apoptosis and miR-505 expression were detected by transfection of lnc-MVIH shRNA and control shRNA into KG-1 cells. And the effect of miR-505 knockdown on lnc-MVIH, cell proliferation, cell apoptosis as well as potential miR-505 target genes [high mobility group box 1 (HMGB1) and cyclin E2 (CCNE2)] in lnc-MVIH knockdown treated KG-1 cells was assessed by transfection of lnc-MVIH shRNA and lnc-MVIH shRNA & miR-505 shRNA into KG-1 cells. Results: Lnc-MVIH expression was elevated in AML-193, KG-1, OCI-AML2 cell lines, but similar in HL-60 cell line compared with primary normal BMMC. Lnc-MVIH knockdown inhibited cell proliferation but promoted cell apoptosis in KG-1 cells, meanwhile miR-505 expression was increased by lnc-MVIH knockdown in KG-1 cells. And in rescue experiments, miR-505 knockdown had no effect on expression of lnc-MVIH, while it increased the expressions of HMGB1 and CCNE2, promoted cell proliferation, inhibited cell apoptosis in lnc-MVIH knockdown treated KG-1 cells.Conclusions: Lnc-MVIH knockdown inhibits cell proliferation but promotes cell apoptosis via regulating miR-505 mediated HMGB1 and CCNE2 in AML.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LncRNA MVIH knockdown inhibits the malignancy progression through downregulating miR-505 mediated HMGB1 and CCNE2 in acute myeloid leukemia

Ke¹,

Zhou²

2019

Transl. Cancer Res.

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“…Additionally, several reports have indicated that miR-505 plays a suppressor role in cervical carcinoma by targeting the Frizzled-4 gene (FZD4) [ 68 ] and in endometrial cancer by targeting transforming growth factor- α (TGF- α ) [ 69 ]. miR-505 expression is correlated with the potential of establishing a biomarker of the imatinib therapeutic response in chronic myeloid leukemia patients [ 70 ]. Interestingly, Qin et al have reported that miR-505 is upregulated in a nasopharyngeal cell line but that miR-505 surprisingly still inhibits metastasis and suppresses the expression of EMT markers, which are the genes associated with cell migration and invasion [ 71 ].…”

Section: Micrornas Regulate Hmgb1 Signaling Pathwaysmentioning

confidence: 99%

MicroRNA-Mediated Regulation of HMGB1 in Human Hepatocellular Carcinoma

Yan

Ying

Cai

2018

BioMed Research International

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High-mobility group box 1 (HMGB1) is a potential therapeutic target and novel biomarker in a variety of malignant tumors, including hepatocellular carcinoma (HCC). More recently, a number of microRNAs (miRNAs) are identified as a class of regulators for broad control of HMGB1-mediated biological actions in eukaryotic cells. In this review article we will describe representative miRNAs involved in regulating the HMGB1 signaling pathways in HCC cell lines and/or animal models. We also propose the possible mechanisms underlying the miRNA/HMGB1 axis and discuss the future clinical significance of miRNAs targeting HMGB1 molecule for HCC therapy.

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“…Recently, the specific role of miR-505-3p in human diseases caught our attention. For example, miR-505 was identified as a potential biomarker for the imatinib response in patients with chronic myeloid leukemia ( 9 ). It has been reported that miR-505 identified endothelial cell migration and tube formation in patients with essential hypertension ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑505‑3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression

2020

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Previous studies have reported that microRNA (miR)-505 exhibits important effect in human cancers. However, the regulatory mechanism of miR-505-3p/high-mobility group box 1 (HMGB1) axis is still unclear in glioma. Therefore, the regulatory mechanism of miR-505-3p/HMGB1 axis in glioma was illuminated. Expression of miR-505-3p and HMGB1 was observed by RT-qPCR. Protein expression was measured by western blot analysis. Dual luciferase assay was performed to confirm the relationship between miR-505-3p and HMGB1. The function of miR-505-3p was investigated by MTT and Transwell assays. Expression of miR-505-3p was reduced in glioma, which was related to poor clinical outcomes and prognosis in glioma patients. Moreover, overexpression of miR-505-3p suppressed proliferation, migration and invasion of glioma cells. In addition, HMGB1 was confirmed as a direct target of miR-505-3p, and miR-505-3p inhibited the development of glioma by targeting HMGB1. Furthermore, miR-505-3p blocked EMT suppressing p-AKT expression in glioma cells. In conclusion, miR-505-3p inhibited the development of glioma by targeting HMGB1 and regulating AKT expression.

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miR-505-5p and miR-193b-3p: potential biomarkers of imatinib response in patients with chronic myeloid leukemia

Cited by 13 publications

References 15 publications

LncRNA MVIH knockdown inhibits the malignancy progression through downregulating miR-505 mediated HMGB1 and CCNE2 in acute myeloid leukemia

LncRNA MVIH knockdown inhibits the malignancy progression through downregulating miR-505 mediated HMGB1 and CCNE2 in acute myeloid leukemia

MicroRNA-Mediated Regulation of HMGB1 in Human Hepatocellular Carcinoma

MicroRNA‑505‑3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression

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