MiR-199a/b-5p inhibits hepatocellular carcinoma progression by post-transcriptionally suppressing ROCK1

Zhan, Yangyang; Zheng, Nanxin; Teng, Fei; Bao, Leilei; Liu, Fang; Zhang, Dongke; Guo, Meng; Guo, Weijian; Ding, Guoyu; Wang, Quanxing

doi:10.18632/oncotarget.18052

Cited by 46 publications

(41 citation statements)

References 46 publications

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“…ROCK1 is involved in the regulation of the PI3K/AKT signalling pathway (28)(29)(30). Hence, we determined the PI3K, p-PI3K, AKT and p-AKT expression levels in Y79 and WERI-RB-1 cells cotransfected with miR-448 mimics and pcDNA3.1 or pcDNA3.1-ROCK1.…”

Section: Mir-448 Suppresses the Pi3k/akt Signalling Pathway In Rbmentioning

confidence: 99%

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Liu

et al. 2018

Oncol Rep

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Retinoblastoma (RB) is the most common primary intraocular malignancy during infancy and childhood worldwide. Numerous microRNAs (miRNAs) contribute to RB initiation and progression through the regulation of cell proliferation, cycle, apoptosis, migration, invasion and metastasis. Therefore, further investigation concerning the expression, roles and associated mechanisms of RB‑related miRNAs may be beneficial to develop novel strategies for patients with this malignancy. Recently, miRNA‑448 (miR‑448) has been reported to be aberrantly expressed and to play an important role in several types of human cancer. However, the expression patterns and biological roles of miR‑448 in RB have not been studied. The aim of the present study was to detect the expression levels of miR‑448 and investigate its functions in RB and its associated molecular mechanisms. In the present study, miR‑448 was significantly downregulated in RB tissues and cell lines. Upregulation of miR‑448 decreased cell proliferation and invasion and increased apoptosis in RB cells. Additionally, ρ‑associated coiled‑coil containing protein kinase 1 (ROCK1) was validated as a novel direct target gene of miR‑448 in RB. ROCK1 was overexpressed in RB tissues and inversely correlated with miR‑448 expression. Furthermore, ROCK1 silencing induced effects on the proliferation, invasion and apoptosis of RB cells similar to those observed following miR‑448 overexpression. Moreover, restoration of miR‑448 expression markedly reversed the effects of miR‑448 overexpression on RB cells, further supporting the hypothesis that ROCK1 is a direct functional target of miR‑448 in RB. Importantly, miR‑448 targeted ROCK1 to inhibit the activation of the PI3K/AKT signalling pathway in RB. These results demonstrated that miR‑448 may serve as a tumour suppressor in RB by directly targeting ROCK1 and regulating the PI3K/AKT signalling pathway, thereby suggesting that miR‑448 may be an effective therapeutic target for treating this aggressive cancer.

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Section: Mir-448 Suppresses the Pi3k/akt Signalling Pathway In Rbmentioning

confidence: 99%

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Liu

et al. 2018

Oncol Rep

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“…Several autophagy-inhibiting miRNAs, namely, miR-23b, miR-24, miR-26, miR-30a, miR-34, miR-125a, miR-141, miR-143, miR-199, miR-200 and miR-520 are found to be downregulated in cancer. Notably, these miRNAs are also known MET effectors [35][36][37][38][39][40][41][42][43][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61]85,86] . As opposed to the primary role(s) of oncomiRs, we speculate that the loss of these miRNAs allows for higher autophagy flux and suppression of MET in the DTCs to help them adapt to unfavorable settlement sites.…”

Section: Autophagy-regulating Mirnas In Cancer Metastasismentioning

confidence: 99%

Micromanaging autophagy with microRNAs to drive cancer metastasis

Eng¹,

Kok²,

Cheong³

2019

JCMT

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While we made great strides in the early detection of a handful of cancers, many other cancers are still detected at fairly later stages, thus hindering the deployment of effective surgical or therapeutic intervention to change their dismal clinical outcomes. The arduous journey of cancer cells from the primary tumor to colonize distant secondary organs or tissues begins with their ability to activate or deactivate various cellular processes at will, including the autophagy machinery. In this review, we discuss how circulatory cancer cells from primary tumors could selectively mobilize different subsets of microRNAs (miRNAs) to enable autophagic recycling of nutrients during their search for secondary sites to colonize and to disable such cell survival programs once they have successfully established at distant organs or tissues. We also discuss how this new miRNA-autophagy-metastasis axis can be targeted by the emerging RNA Medicine toolkit.

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“…According to our previous method [14], the obtained proteins were quantified by the BCA (Thermo Fisher Scientific, Waltham, MA, USA) method. After denaturation, equal amounts of proteins (500 ng/µL, 10 µL) from different samples were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to nitrocellulose membranes (Millipore).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…In our previous study, we found that the expression of miRNA miR-500a was significantly increased in HCC as compared to normal liver according to heat map analysis of RNA sequencing in The Cancer Genome Atlas (TCGA) database [14]. Also, previous studies have shown that miR-500a is of great interest in cancer therapies due to its association with various types of cancer, including gastric cancer [15] and prostate cancer [16].…”

Section: Introductionmentioning

confidence: 98%

“…Functional studies have confirmed that miRNAs play vital roles in various important biological processes, including proliferation, differentiation, apoptosis, and migration; thus, they have important roles in the properties of cancer biology and may serve as potential therapeutic targets [7,11,12]. For HCC, a set of deregulated miRNAs has been shown to participate in its carcinogenesis and progression, and the miRNome study in HCC tissues suggested some important deregulated miRNAs in HCC cancer biology, such as miR-361 [8], miR-122 [13], and miR-199 [14]. However, as multiple miRNAs are deregulated in cancer cells and a single miRNA can target multiple mRNAs, identifying the deregulated miRNAs in HCC and uncovering their roles in HCC development is an ongoing process.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-500a Promotes the Progression of Hepatocellular Carcinoma by Post-Transcriptionally Targeting BID

Bao

Zhang

Han

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatocellular carcinoma (HCC) is one of the most common human malignant diseases in the world, and the mechanisms underlying HCC carcinogenesis and progression need further investigation. MicroRNAs play important roles in the development of cancer, and miR-500a is suggested to be deregulated in some types of cancer. However, the underlying molecular mechanisms of miR-500a in HCC remain unknown. Methods: The expression of miR-500a in HCC was analyzed in The Cancer Genome Atlas (TCGA) database and examined in 33 pairs of HCC tissues and matched nontumor tissues. The correlation between miR-500a expression and prognosis of HCC patients was analyzed from the survival data in TCGA. The mechanism of miR-500a upregulation in HCC was detected using chromatin immunoprecipitation-quantitative real-time PCR. The roles of miR-500a in HCC development were examined using a cell counting kit-8 assay in vitro and growth of transplanted tumors in nude mice in vivo. Apoptosis of HCC was detected using Annexin V/propidium iodide staining. The expression of BH3-interacting death agonist (BID) protein was examined using western blot analysis. Results: miR-500a expression was upregulated in HCC tissues, and high miR-500a expression was significantly correlated with the poor prognosis of HCC patients. Histone modifications in the promoter region of miR-500a may be responsible for its increased expression. Inhibition of miR-500a in HCC cell lines significantly promoted apoptosis, as well as inhibiting the proliferation of HCC cells and growth of transplanted tumors in nude mice. miR-500a directly targeted the 3′ untranslated region of BID mRNA, and inhibition of miR-500a-promoted apoptosis was almost completely abolished by the administration of ABT-199 via the BID-mitochondria pathway. Conclusion: Our results suggest that histone modifications in the promoter region of miR-500a may be responsible for the increased expression of miR-500a in HCC, which promotes cancer progression by targeting BID, indicating that miR-500a may be a potential prognostic predictor and therapeutic target for HCC patients.

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MiR-199a/b-5p inhibits hepatocellular carcinoma progression by post-transcriptionally suppressing ROCK1

Cited by 46 publications

References 46 publications

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

MicroRNA‑448 inhibits the progression of retinoblastoma by directly targeting ROCK1 and regulating PI3K/AKT signalling pathway

Micromanaging autophagy with microRNAs to drive cancer metastasis

MicroRNA-500a Promotes the Progression of Hepatocellular Carcinoma by Post-Transcriptionally Targeting BID

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