microRNA-19a-3p promotes tumor metastasis and chemoresistance through the PTEN/Akt pathway in hepatocellular carcinoma

Jiang, Xuemei; Yu, Xiang‐Nan; Liu, Taotao; Zhu, Hongxia; Shi, Xuan; Bilegsaikhan, Enkhnaran; Guo, Huimin; Song, Guangqi; Weng, Shuqiang; Huang, Xiaoxi; Dong, Ling; Janssen, Harry L A; Shen, Xizhong; Zhu, Ji‐Min

doi:10.1016/j.biopha.2018.06.097

Cited by 91 publications

(63 citation statements)

References 40 publications

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“…MicroRNAs (miRs), 21-22 nucleotides long, are short noncoding RNAs and are known to function in post-transcriptional regulation of gene expression through majorly binding the 3′-untranslated region (UTR) of their target messenger RNA (mRNA), accordingly modulating cells' behaviors [13,14]. The broadly conserved miR-19a-3p, a crucial component of the miR-17-92 cluster, has been shown to be involved in pathogenesis/disease progression in lung cancer [15], gastric cancer [16], breast cancer [17], and hepatocellular carcinoma [18]. Furthermore, miR-19a-3p has been found to be overexpressed in glioma cells and astrocytic glioma tissues and its overexpression is strongly linked with malignancy grades in glioma patients, indicating an important role in gliomagenesis [19].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR-19a protects neurons against ischemic stroke through modulating glucose metabolism and neuronal apoptosis

Wang

Liu

et al. 2019

Cell Mol Biol Lett

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Background: Accumulating evidence has shown that altered microRNA (miR) modulation is implicated in the pathologies of ischemic stroke. However, it is unclear whether and how hsa-miR-19a-3p mediates cerebral ischemic injury. Herein, we investigated the functional role of miR-19a-3p in cerebral ischemic injury and explored its underlying regulatory mechanism. Methods: In vivo ischemic/reperfusion (I/R) neuronal injury and in vitro oxygenglucose deprivation (OGD) were established. Expression of miR-19a-3p was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Glucose uptake, lactate production, and apoptosis were determined. ADIPOR2 was predicted as a target of miR-19a-3p in silico and experimentally validated by qRT-PCR, Western blot analysis and luciferase assay assays. Results: MiR-19a expression was significantly downregulated and upregulated in rat neurons and astrocytes, respectively (P < 0.01). A significantly elevated level of miR-19a-3p was found in I/R and OGD models in comparison to sham/control groups (P < 0.01). Expression of the glycolysis enzyme markers LDHA, PKM2, HK2, Glut1 and PDK1, apoptosis-related factors levels, apoptosis, glucose uptake, and lactate production were significantly repressed by both I/R and OGD (P < 0.01 in each case). Moreover, miR-19a-3p mimic aggravated, while miR-19a-3p inhibitor alleviated, the above observations. Adipor2 was predicted and confirmed to be a direct target of miR-19a. Furthermore, restoration of Adipor2 reversed miR-19a-3p-induced effects. Conclusions: Collectively, our results indicate that elevated miR-19a-3p mediates cerebral ischemic injury by targeting ADIPOR2. MiR-19a-3p attenuation thus might offer hope of a novel therapeutic target for ischemic stroke injury treatment.

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Section: Introductionmentioning

confidence: 99%

Inhibition of miR-19a protects neurons against ischemic stroke through modulating glucose metabolism and neuronal apoptosis

Wang

Liu

et al. 2019

Cell Mol Biol Lett

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“…Accumulating evidence suggested that miRNAs play important roles in the initiation and progression of various human cancers including ovarian cancer . miR‐19a‐3p is a member of the miR‐17 to 92 clusters, its expression is frequently dysregulated and which is closely associated with proliferation, apoptosis, metastasis, and chemoresistance of various malignant tumors such as gastric cancer, pancreatic cancer, liver cancer, lung cancer and breast cancer . It has been reported that miR‐19a was highly expressed in ovarian cancer tissues and cell lines, and it promotes the growth of ovarian cancer cells …”

Section: Introductionmentioning

confidence: 99%

The NF‐κB‐modulated miR‐19a‐3p enhances malignancy of human ovarian cancer cells through inhibition of IGFBP‐3 expression

Bai

Cui

et al. 2019

Molecular Carcinogenesis

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Ovarian cancer is the most lethal gynecologic malignancy due to the lack of symptoms until advanced stages, and new diagnosis and treatment strategy is in urgent need. In this study, we found higher expression of miR‐19a‐3p in ovarian cancer tissues compared with that in the adjacent normal tissues. By chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) analysis, we showed that nuclear factor‐kappaB (NF‐κB) binds to the promoter of miR‐19a‐3p, leading to reduced expression in ovarian cancer cells. Further study indicated that miR‐19a‐3p inhibits the expression of insulin‐like growth factor binding protein‐3 (IGFBP‐3), resulting in enhanced growth and migration of ovarian cancer cells in vitro and tumor growth in vivo. These results showed that miR‐19a‐3p enhances the oncogenesis of ovarian cancer through inhibition of IGFBP‐3 expression, and which can be inhibited by NF‐κB, suggesting an NF‐κB/miR‐19a‐3p/IGFBP‐3 pathway in the oncogenesis of ovarian cancer, which expands our understanding of ovarian cancer and they may contribute to the development of new diagnosis and treatment of ovarian cancer.

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“…MiR-19a-3p functioned as an oncogene or a tumor suppressor in various cancers. For example, miR-19a-3p is distinctly increased in hepatocellular carcinoma (HCC), and promotes HCC cell metastasis and chemoresistance [31]. In contrast, miR-19a-3p expression is reduced in osteosarcoma, and silencing miR-19a-3p suppresses osteosarcoma cell proliferation and induces apoptosis [32].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

Shen

Wang

et al. 2020

Preprint

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Background Long intergenic non-protein coding RNA 00342 (LINC00342) has been identified as a novel oncogene. However, the functional role of LINC00342 in colorectal cancer (CRC) remains unclear. Methods The expression of LINC00342 was detected by real-time PCR. Cell proliferation, migration and invasion and xenograft model were examined to analyze the biological functions of LINC00342 in vitro and in vivo. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to identify the target interactions between LINC00342, miR-19a-3p and aminopeptidase like 1 (NPEPL1). Results LINC00342 was highly expressed in CRC. Downregulation of LINC00342 inhibited cell proliferation and metastasis of CRC cells. Moreover, knocking down LINC00342 could weaken the tumor growth in vivo. Mechanistic investigation revealed that LINC00342 might sponge miR-19a-3p to regulate NPEPL1 expression. Further investigation indicated that the oncogenesis facilitated by LINC00342 was inhibited due to the depletion of NPEPL1.Conclusion LINC00342 promoted CRC progression by competitively binding miR-19a-3p with NPEPL1.

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microRNA-19a-3p promotes tumor metastasis and chemoresistance through the PTEN/Akt pathway in hepatocellular carcinoma

Cited by 91 publications

References 40 publications

Inhibition of miR-19a protects neurons against ischemic stroke through modulating glucose metabolism and neuronal apoptosis

Inhibition of miR-19a protects neurons against ischemic stroke through modulating glucose metabolism and neuronal apoptosis

The NF‐κB‐modulated miR‐19a‐3p enhances malignancy of human ovarian cancer cells through inhibition of IGFBP‐3 expression

LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1

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