MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2

Ke, Shun; Li, Ruichao; Lü, Jun; Meng, Fankai; Feng, Yun‐Zhi; Fang, Minghao

doi:10.1007/s12185-017-2232-2

Cited by 33 publications

(19 citation statements)

References 30 publications

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“…In line with our results, miR-192 has been reported to inhibit cell proliferation and induce apoptosis in vitro 39,40 and rheumatoid arthritis 41 . Also, p53 can induce miR-192 to promote its activation facilitating cell cycle arrest 42,43 .…”

Section: Discussionsupporting

confidence: 92%

New signatures of poor CD4 cell recovery after suppressive antiretroviral therapy in HIV-1-infected individuals: involvement of miR-192, IL-6, sCD14 and miR-144

Hernández-Walias

Ruiz-de-León

Rosado‐Sánchez

et al. 2020

Sci Rep

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Up to 40% of newly diagnosed cases of HIV-1 infection are late diagnoses, with a profound decrease in CD4 cell counts in many cases. One-third of these individuals do not achieve optimal CD4 cell recovery (OR) after suppressive antiretroviral treatment (ART). This retrospective/longitudinal study of poor recovery (PR) included 79 HIV-1-infected individuals with CD4 count <200 cells/mm 3 (25 PR and 54 OR) before ART. After suppressive ART, 21 PR and 24 OR individuals were further analysed, including paired samples. Selected miRs and plasma inflammatory markers were determined to investigate their potential predictive/diagnostic value for poor recovery. miR-192, IL-6 and sCD14 were independently associated with CD4 recovery before ART (p = 0.031, p = 0.007, and p = 0.008, respectively). The combination of these three factors returned a good discrimination (predictive value for pR) value of 0.841 (AUC, p < 0.001). After suppressive ART, miR-144 was independently associated with CD4 recovery (p = 0.017), showing a moderate discrimination value of 0.730 (AUC, p = 0.008) for PR. Our study provides new evidence on the relationship between miRs and HIV-1 infection that could help improve the management of individuals at HIV-1 diagnosis. These miRs and cytokines signature sets provide novel tools to predict CD4 cell recovery and its progression after ART.Newly diagnosed cases of HIV-1 infection include individuals with a late diagnosis who often have a low level of CD4 cell counts. Antiretroviral treatment (ART) can restore the CD4 cell level in most of the HIV-1-infected individuals. Nevertheless, one-third of these individuals remained at a very low CD4 level (<200 cells/mm 3 ) after ART despite virological suppression 1-3 .Persistent immune activation and inflammation are associated with poor CD4 cell recovery (PR). These factors contribute to the risk of illness, increasing the risk of several morbidities compared to the uninfected population, as well as the risk of death 4,5 . While to date no effective alternative treatment is available to increase the CD4 cell levels to optimal counts, initiation of ART early after HIV-1 diagnosis might provide a good opportunity to maximise the CD4 cell recovery.On the other hand, adding antiretroviral drugs to an already suppressive treatment does not improve either CD4 cell recovery nor reduce morbidity or mortality 6,7 . Besides, no observable clinical benefit was observed in

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Section: Discussionsupporting

confidence: 92%

New signatures of poor CD4 cell recovery after suppressive antiretroviral therapy in HIV-1-infected individuals: involvement of miR-192, IL-6, sCD14 and miR-144

Hernández-Walias

Ruiz-de-León

Rosado‐Sánchez

et al. 2020

Sci Rep

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“…Although several studies have shown that miR-192 could target YY1, CCNT2, and GATA6 in human cancers, the mechanism of miR-192 in regulating PCa progression remains unclear [28, 29]. In the present study, we performed bioinformatics analysis for miR-192–5p to explore its potential mechanisms in PCa by using its targets.…”

Section: Discussionmentioning

confidence: 99%

miR-192 Is Overexpressed and Promotes Cell Proliferation in Prostate Cancer

et al. 2018

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Objective: Prostate cancer (PCa) is one of the most prevalent types of cancer among men worldwide. The incidence of PCa is increasing in China. Therefore, there is an urgent need to identify novel diagnostic and prognostic markers for PCa to improve the treatment of the disease. Methods: The Cancer Genome Atlas (TCGA) and GEO database were used to analyze the expression of miR-192, and the relationship between miR-192 and the clinical features of patients with PCa. Cell cycle and cell proliferation assay were used to detect the functional roles of miR-192 in PCa. Bioinformatic analysis for miR-192–5p was performed using gene ontology and KEGG analysis. Results: By analyzing the dataset of TCGA, we found that miR-192 was overexpressed in PCa samples compared to normal tissues and was upregulated in high-grade PCa compared to low-grade PCa. We also observed that higher miR-192 expression was associated with a shorter biochemical recurrence-free survival time. Our results also demonstrated that miR-192 promoted PCa cell proliferation and cell cycle progression. Conclusion: These results suggest that miR-192 may be considered for use as a potential diagnostic and therapeutic target of PCa.

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“…miRNAs can act as oncogenes or anti-oncogenes, facilitating cancer initiation and progression in solid and hematological malignancies [9]. Functionally, the implication of several miRNAs in fundamental biological processes has been identified in AML, such as apoptosis (miR-29b [10] and miR-149-5p [11]), differentiation (miR-155 [12]), cell cycle and proliferation (miR-125a [13] and miR-192 [14]). Recently, the distorted and unique expression pattern of miR-362-5p in several types of malignant tumor coupled with its abnormal expression in keeping the malignant phenotype of cancer cells make miR-362-5p a novel molecular target for regulation and detection [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

Chen

et al. 2020

Human Cell

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Recently, miR-362-5p has attracted special interest as a novel prognostic predictor in acute myeloid leukemia (AML). However, its biological function and underlying molecular mechanism in AML remain to be further defined. Herein, we found that a significant increase in miR-362-5p expression was observed in AML patients and cell lines using quantitative realtime PCR. The expression of miR-362-5p was altered in THP-1 and HL-60 cells by transfecting with miR-362-5p mimic or inhibitor. A series of experiments showed that inhibition of miR-362-5p expression significantly suppressed cell proliferation, induced G0/G1 phase arrest and attenuated tumor growth in vivo. On the contrary, ectopic expression of miR-362-5p resulted in enhanced cell proliferation, cell cycle progression and tumor growth. Moreover, growth arrest-specific 7 (GAS7) was confirmed as a direct target gene of miR-362-5p and was negatively modulated by miR-362-5p. GAS7 overexpression imitated the tumor suppressive effect of silenced miR-362-5p on THP-1 cells. Furthermore, miR-362-5p knockdown or GAS7 overexpression obviously down-regulated the expression levels of PCNA, CDK4 and cyclin D1, but up-regulated p21 expression. Collectively, our findings demonstrate that miR-362-5p exerts oncogenic effects in AML by directly targeting GAS7, which might provide a promising therapeutic target for AML.

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MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2

Cited by 33 publications

References 30 publications

New signatures of poor CD4 cell recovery after suppressive antiretroviral therapy in HIV-1-infected individuals: involvement of miR-192, IL-6, sCD14 and miR-144

New signatures of poor CD4 cell recovery after suppressive antiretroviral therapy in HIV-1-infected individuals: involvement of miR-192, IL-6, sCD14 and miR-144

miR-192 Is Overexpressed and Promotes Cell Proliferation in Prostate Cancer

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia

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