The Long Noncoding RNA TTTY15, Which Is Located on the Y Chromosome, Promotes Prostate Cancer Progression by Sponging let-7

Xiao, Guangan; Yao, Jiayi; Kong, De-Pei; Wang, Hongzhi; Chen, Rui; Li, Li; Zeng, Tao; Wang, Liujun; Zhang, Wei; Shi, Xiaolei; Zhou, Tie; Li, Jing; Wang, Yue; Xu, Chuan; Jiang, Junfeng; Sun, Yinghao

doi:10.1016/j.eururo.2018.11.012

Cited by 68 publications

(58 citation statements)

References 42 publications

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“…acted as a ceRNA and negatively regulated miR-let-7 to promote expression of the target genes (CDK6, FN1) [38]. In recent years, mounting studies have shown that lncRNA, acting as ceRNA, regulated the expression of downstream oncogenes and tumor suppressor genes in endometrial carcinoma through a miRNA regulatory mechanism.…”

Section: Resultsmentioning

confidence: 99%

Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

Gao

Nie

Zhang

et al. 2020

Preprint

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Background: Endometrial carcinoma (EC) is one of the most common malignant tumors in gynecology. The potential functions and mechanisms of long noncoding RNAs (lncRNAs) in the occurrence and progression of EC remains unclear. It’s meaningful to explore lncRNAs signature for providing prognostic value of EC. Methods：The differentially expressed lncRNAs and their prognostic values in EC were investigated based on The Cancer Genome Atlas (TCGA) database; the transcriptional factors (TFs), the competing endogenous RNA (ceRNA) mechanism, functional regulatory network and immune infiltration of RP11-89K21.1 and RP11-357H14.17 were further explored by various bioinformatics tools and databases. Results: We firstly identified high expression of RP11-89K21.1 and RP11-357H14.17 were closely associated with shorten overall survival (OS) and poor prognosis in patients with EC. We also elucidated the networks of transcription factor and co-expression genes associated with RP11-89K21.1 and RP11-357H14.17. Furthermore, the ceRNA network mechanism was successfully constructed through 2 lncRNAs (RP11-89K21.1 and RP11-357H14.17), 11 miRNAs and 183 mRNAs. Functional enrichment analysis revealed that the targeting genes of RP11-89K21.1 and RP11-357H14.17 were strongly associated with microRNAs in cancer, vessel development, growth regulation, growth factor and cell differentiation, and involved in pathways including pathways in cancer, microRNAs in cancer and apoptotic signaling pathway. Conclusions: We demonstrated for the first time that RP11-89K21.1 and RP11-357H14.17 may play crucial roles in the occurrence, development and malignant biological behavior of EC, and can be regarded as potential prognostic biomarkers for EC.

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Section: Resultsmentioning

confidence: 99%

Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

Gao

Nie

Zhang

et al. 2020

Preprint

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“…As an important family of miRNAs, let-7b-5p participates in the growth, proliferation, invasion, and metastasis of cancer by regulating the expression of a variety of oncogenes and cytokines 24 . Speci cally, let-7a, let-7b, and let-7c have been identi ed as potential tumor suppressors that directly target the mRNAs of genes involved in the cell cycle and signal transduction pathways that contribute to the initiation and development of PCa 25,26 . Let-7c is also associated with macrophage differentiation 27 , but the role of let-7b-5p in the shift of M1/M2 in PCa has been largely unde ned.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of let-7b-5p contributes to anti-tumorigenic macrophage phenotype through SOCS1/STAT pathway in prostate cancer

Rong

et al. 2020

Preprint

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BackgroundDysfunction of microRNAs (miRNAs) is a major cause of aberrant expression of inflammatory cytokines and contributes to macrophage polarization. Previous studies have shown that miRNA let-7 is associated with cell differentiation, and the expression of let-7b-5p is significantly increased in M2 macrophages. However, the mechanism by which let-7b-5p regulates macrophage differentiation in prostate cancer (PCa) remains largely unknown.MethodsHuman macrophages were induced by the blood monocytes from healthy male donors. M1 macrophages were polarized by stimulating overnight with 100 ng/ml lipopolysaccharides and 100 ng/ml IFN-γ, while conditioned medium from PC-3 cells were used to induce prostatic macrophages (M-CMs) in vitro, and then let-7b-5p mimics or inhibitors were transfected into M1 and M-CMs for 72 hours respectively. The expression of cluster of differentiation 206 (CD206) in each group was detected by a High Throughput Connotation of Imaging System. Quantitative real-time polymerase chain reaction (qRT-PCR) was executed to examine the expression of inflammatory cytokines IL-10, IL-12, IL-13, TNF-alpha and let-7b in macrophages. SOCS1 protein level was evaluated by ELISA, and the phosphorylation difference of STAT family member proteins was analysized by CST signal pathway chip. Phagocytosis of macrophages and the effect of macrophages on the proliferation of prostate cancer cell PC-3 were evaluated by phagocytosis assay or Cell Counting Kit-8 (CCK-8). The relationship between SOCS1 and let-7b-5p was confirmed with the dual-luciferase reporter.ResultsThe expression of cluster of differentiation 206 (CD206), an M2-like macrophage surface molecule, was significantly increased in M1 macrophages treated with let-7b-5p mimics, while CD206 expression was decreased in M-CMs treated with let-7b-5p inhibitors. Overexpression or knockdown of let-7b-5p significantly affected the expression of inflammatory factors in macrophages including interleukin 10 (IL-10), IL-12, IL-13, and tumor necrosis factor alpha. Let-7b-5p downregulated the expression of suppressor of cytokine signaling 1 (SOCS1) and increased the phosphorylation of signal transducer and activator of transcription 1 (STAT1), STAT3, and STAT5a proteins in M-CMs and M1 macrophages with let-7b-5p mimics compared with the other groups. In addition, with high expression of let-7b-5p, the phagocytosis of macrophages showed a significant decrease. As a result, M-CMs treated with let-7b-5p inhibitors reduced the proliferation of PC-3 PCa cells.ConclusionsCollectively, these data indicate that let-7b-5p may regulate M2 polarization through the SOCS1/STAT pathway, and reversal of M2 differentiation by let-7b-5p inhibitors can enhance macrophage phagocytosis, ultimately inhibiting the proliferation of PCa cells.Trial registrationNot applicable

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“…The competing endogenous RNA (ceRNA) mechanism is a recently reported RNA-RNA interaction model which is theoretically common in many bioprocesses [18][19][20]. Indeed, ceRNA mechanisms have been reported to be involved in development, cancer, and plenty of other situations [33][34][35]. However, whether this mechanism was related to hepatic IRI was unknown until now.…”

Section: Discussionmentioning

confidence: 99%

lncRNA AK054386 Functions as a ceRNA to Sequester miR-199 and Induce Sustained Endoplasmic Reticulum Stress in Hepatic Reperfusion Injury

Dai

Qiao

Zhang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hepatic ischemia-reperfusion injury (IRI) is a very complex pathological process that is often associated with liver trauma and surgery, especially liver transplantation surgery. Although endoplasmic reticulum stress (ERS) plays a role in this process, the posttranscriptional regulators and the underlying mechanisms are still unclear. Here, we report that the lncRNA AK054386 was increased in hepatic IRI models. Furthermore, AK054386 can act as a “competing endogenous RNA (ceRNA)” and regulate ERS-related factors by binding and sequestering miR-199, which was shown to inhibit ERS in our previous report. Increased expression of AK054386, which might be mediated by activated NF-κB, resulted in sustained ERS and increased cell apoptosis and death in hepatic IRI mouse and cellular models. In contrast, AK054386 inhibition had protective effects on these models. Our data indicate that AK054386 and miR-199 are critical players in hepatic IRI, and we broadened the scope regarding ceRNA mechanisms. We hope that our results will improve the understanding of hepatic IRI and may provide potential therapeutic targets.

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The Long Noncoding RNA TTTY15, Which Is Located on the Y Chromosome, Promotes Prostate Cancer Progression by Sponging let-7

Cited by 68 publications

References 42 publications

Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

Inhibition of let-7b-5p contributes to anti-tumorigenic macrophage phenotype through SOCS1/STAT pathway in prostate cancer

lncRNA AK054386 Functions as a ceRNA to Sequester miR-199 and Induce Sustained Endoplasmic Reticulum Stress in Hepatic Reperfusion Injury

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