&lt;p&gt;MiR-155-5p accelerates the metastasis of cervical cancer cell via targeting TP53INP1&lt;/p&gt;

Li, Ning; Tao, Cui; Guo, Wenbin; Wang, Dianwei; Mao, Li

doi:10.2147/ott.s193097

Cited by 74 publications

(54 citation statements)

References 34 publications

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“…miR-155 is previously identified as an oncogenic miRNA in various cancers, such as breast cancer, ovarian cancer and lung cancer. [32][33][34] In our work, we observed that miR-155 was upregulated in both M2 TAMs and exosomes secreted by M2 TAMs. Moreover, the function of exosomes secreted by M2 TAMs in NSCLC metastasis was mediated by miR-155, which modulated RASSF4 in NSCLC cells.…”

Section: Discussionsupporting

confidence: 53%

Tumor-associated macrophages secret exosomal miR-155 to promote metastasis of non-small-cell lung cancer

Chen

et al. 2020

Preprint

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Background: Understanding the molecular basis underlying metastasis of non-small-cell lung cancer (NSCLC) may provide new therapeutic modality for treatment of NSCLC. However, the mechanisms by which tumor-associated macrophages (TAMs) affect NSCLC metastasis still remain undefined. Method: Phenotype of TAMs was identified by flow cytometry. The migration of the tumor cells was detected by transwell assay. Transmission electron microscopy (TEM) and PKH-67 was used to identified and label the exosome. Expression of miR-155 was measured by qRT-PCR. Luciferase analysis, western blot, and rescue assay were used to investigate potential mechanisms of miR-155.Results: We discovered a novel regulatory pathway involved in NSCLC metastasis. We found that M2 TAMs were the main TAMs in metastatic tissues of NSCLC patients and exosomes derived from M2 TAMs were able to promote epithelial-mesenchymal transition (EMT) and migration of NSCLC cells. We demonstrated that miR-155 was abundant in M2 TAMs and exosomes secreted by M2 TAMs. Moreover, we also verified that miR-155 was the key functional biomolecule in exosomes secreted by M2 TAMs. Furthermore, we confirmed that deletion of miR-155 in M2 TAMs could significantly prevent NSCLC metastasis. Overall, Conclusions: we revealed a new regulatory pathway that is M2 TAMs secret exosomal miR-155 to promote NSCLC metastasis. Our findings may provide a practical target for treatment of NSCLC.

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Section: Discussionsupporting

confidence: 53%

Tumor-associated macrophages secret exosomal miR-155 to promote metastasis of non-small-cell lung cancer

Chen

et al. 2020

Preprint

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“…Recently, the involvement of miRNAs in tumorigenesis and their signi cance as effective biomarkers are also becoming increasingly appreciated [14]. miR-155-5p has been found to regulate the development of various cancer types, including human epithelial ovarian cancer [16], cervical cancer [17,18], and colon cancer [19]. It has been reported that some certain long non-coding RNAs (lncRNAs) suppress HCC development by sponging miR-155-5p [20]; miR-155-5p modulated the malignancy of HCC by regulating Wnt/β-catenin signaling or suppressing PTEN through the PI3K/Akt pathway [21,22]; therefore, miR-155-5p can be a promising therapeutic target for HCC patients.…”

Section: Discussionmentioning

confidence: 99%

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

Wang

Che

2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is the leading cause of tumor-related death worldwide due to high morbidity and mortality, yet still lacking biomarkers and therapies. Circular RNAs (circRNAs) are a group of non-coding RNAs that regulate gene expression through interacting with miRNAs, implicating in the tumorigenesis and progression. A novel circRNA, circTP63, was reported to be an oncogene in HCC. However, its role in HCC remains unclear.Methods: qRT-PCR was used to assess the mRNA levels of CircTP63 in 90 pairs of tumor and adjacent normal tissues from HCC patients, one human normal hepatic epithelial cell line and HCC cell lines. CCK-8, colony formation, transwell, and flow cytometry assays were performed to detect the cellular function of circTP63/miR-155-5p/ZBTB18 in HCC cells. Bioinformatic analysis, RNA pull-down and luciferase assays were used to determine the interaction among circTP63/miR-155-5p/ZBTB18. Results: circTP63 was significantly upregulated in HCC tissues and cell lines. High circTP63 expression is closely associated with the tumor stages, lymph node metastasis, and poor prognosis of HCC patients. Functionally, knockdown of circTP63 inhibited cell proliferation, migration, invasion, and promoted cell apoptosis of HCC. Meanwhile, overexpression of circTP63 enhanced HCC progression. Mechanically, circTP63 was a sponge of miR-155-5p to facilitate the ZBTB18 expression, and the ZBTB18 expression in HCC tissues was negatively associated with the survival rate of HCC patients. Furthermore, the reduced tumor-promoting effect on HCC cells induced by knockdown of circTP63 can be reversed by miR-155-5p inhibitor or ZBTB18 overexpression. Conclusion: Our data highlight a critical circTP63-miR-155-5p-ZBTB18 regulatory network involved in the HCC progression, gaining mechanistic insights into the function of CircRNAs in HCC progression, and providing effective biomarkers and therapeutic targets for HCC treatment.

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“…[ 20 ] In cervical cancer, miR-155 promotes malignant tumor cell phenotypes through direct targeting of TP53INP1. [ 21 ] Additionally, miR-155 is overexpressed in AML and was identified as a potential biomarker for detecting AML. [ 22 ] Wang [ 23 ] et al demonstrated that miR-146a can promote cell proliferation and suppresses cell apoptosis via the downregulation of CNTFR in AML and ALL.…”

Section: Discussionmentioning

confidence: 99%

Microarray analysis of differentially expressed microRNAs in myelodysplastic syndromes

et al. 2020

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Background: Our study aimed to analyze differential microRNA expression between myelodysplastic syndromes (MDS) and normal bone marrow, and to identify novel microRNAs relevant to MDS pathogenesis. Methods: MiRNA microarray analysis was used to profile microRNA expression levels in MDS and normal bone marrow. Quantitative real-time polymerase chain reaction was employed to verify differentially expressed microRNAs. Results: MiRNA microarray analysis showed 96 significantly upregulated (eg, miR-146a-5p, miR-151a-3p, miR-125b-5p) and 198 significantly downregulated (eg, miR-181a-2-3p, miR-124-3p, miR-550a-3p) microRNAs in MDS compared with normal bone marrow. The quantitative real-time polymerase chain reaction confirmed the microarray analysis: expression of six microRNAs (miR-155-5p, miR-146a-5p, miR-151a-3p, miR-221-3p, miR-125b-5p, and miR-10a-5p) was significantly higher in MDS, while 3 microRNAs (miR-181a-2-3p, miR-124-3p, and miR-550a-3p) were significantly downregulated in MDS. Bioinformatics analysis demonstrated that differentially expressed microRNAs might participate in MDS pathogenesis by regulating hematopoiesis, leukocyte migration, leukocyte apoptotic process, and hematopoietic cell lineage. Conclusions: Our study indicates that differentially expressed microRNAs might play a key role in MDS pathogenesis by regulating potential relevant functional and signaling pathways. Targeting these microRNAs may provide new treatment modalities for MDS.

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<p>MiR-155-5p accelerates the metastasis of cervical cancer cell via targeting TP53INP1</p>

Cited by 74 publications

References 34 publications

Tumor-associated macrophages secret exosomal miR-155 to promote metastasis of non-small-cell lung cancer

Tumor-associated macrophages secret exosomal miR-155 to promote metastasis of non-small-cell lung cancer

CircTP63 Promotes Hepatocellular Carcinoma Progression by Sponging miR-155-5p and Upregulating ZBTB18

Microarray analysis of differentially expressed microRNAs in myelodysplastic syndromes

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