MiR-511 inhibits growth and metastasis of human hepatocellular carcinoma cells by targeting PIK3R3

Cao, Gang; Dong, Weihua; Meng, Xiaoxi; Liu, Hongchao; Liao, Huaqiang; Liu, Shiyuan

doi:10.1007/s13277-015-3085-z

Cited by 39 publications

(34 citation statements)

References 31 publications

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“…lncRNA-PAGBC requires miR-133b and miR-511 to promote growth and metastasis and activate the AKT/mTOR pathway in GBC cells Fig S2, miR-133b and miR-511 could strongly inhibit the proliferation, colony formation and metastasis abilities of GBC cells. Both SOX4 and PIK3R3 have been shown to promote proliferation and metastasis in other carcinomas in previous studies [18][19][20][21]. Moreover, these studies demonstrated that both SOX4 and PIK3R3 are involved with the AKT/mTOR pathway, which is critical for tumour proliferation and metastasis.…”

Section: Lncrna-pagbc Upregulates Sox4 and Pik3r3 Levelsmentioning

confidence: 83%

“…Maybe it can also happen to lncRNAs when they work as ceRNAs in cytoplasm. Additionally, SOX4 and PIK3R3, which are target genes of these two miRNAs and have been identified as oncogenic genes in other malignancies [18][19][20][21], were found to be positively regulated by lncRNA-PAGBC. Again, as expected, this positive relationship was demonstrated to depend on the competitive role of two miRNAs, at least in part.…”

Section: Discussionmentioning

confidence: 99%

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Lnc RNA ‐ PAGBC acts as a micro RNA sponge and promotes gallbladder tumorigenesis

Wang

et al. 2017

EMBO Reports

191

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Long noncoding RNAs (lncRNAs) play roles in the development and progression of many cancers; however, the contributions of lncRNAs to human gallbladder cancer (GBC) remain largely unknown. In this study, we identify a group of differentially expressed lncRNAs in human GBC tissues, including prognosis-associated gallbladder cancer lncRNA (lncRNA-PAGBC), which we find to be an independent prognostic marker in GBC Functional analysis indicates that lncRNA-PAGBC promotes tumour growth and metastasis of GBC cells. More importantly, as a competitive endogenous RNA (ceRNA), lncRNA-PAGBC competitively binds to the tumour suppressive microRNAs miR-133b and miR-511. This competitive role of lncRNA-PAGBC is required for its ability to promote tumour growth and metastasis and to activate the AKT/mTOR pathway. Moreover, lncRNA-PAGBC interacts with polyadenylate binding protein cytoplasmic 1 (PABPC1) and is stabilized by this interaction. This work provides novel insight on the molecular pathogenesis of GBC.

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Section: Lncrna-pagbc Upregulates Sox4 and Pik3r3 Levelsmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Lnc RNA ‐ PAGBC acts as a micro RNA sponge and promotes gallbladder tumorigenesis

Wang

et al. 2017

EMBO Reports

191

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“…Our results showed that miR-511 overexpression significantly decreased the expression of p-Akt, β-catenin, c-Myc and cyclinD1, suggesting that miR-511 acts as a negative regulator of these two pathways. Previous study also showed that miR-511 acts as a negative regulator of PI3K/AKT pathway in liver cancer [38]. Further findings showed overexpression of TRIM24 lacking its 3′-UTR significantly restored PI3K/AKT and Wnt/β-catenin pathways in miR-511-transfected GC cells.…”

Section: Discussionmentioning

confidence: 71%

Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer

Fang

Zhang

Liao

et al. 2017

J Exp Clin Cancer Res

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BackgroundIncreasing evidence highlights the important roles of tripartite motif containing 24 (TRIM24) in tumor initiation and malignant progression in many tumors, including gastric cancer (GC). Although TRIM24 expression is remarkably upregulated during GC carcinogenesis, the molecular mechanisms underlying TRIM24 dysregulation remain unexplored.MethodsIn this study, miRNA target prediction tools were applied to explore miRNAs that potentially target TRIM24. Western blot and quantitative reverse-transcriptase PCR (qRT-PCR) were performed to detected TRIM24 and miR-511 expression in GC tissues and cell lines. Dual-luciferase reporter assay was utilized to validate if TRIM24 is a direct target gene of miR-511. CCK-8 assay, cell colony formation assay, EdU incorporation assay and cell cycle analysis were performed to determine whether miR-511-mediated regulation of TRIM24 could affect GC progression.ResultsIn our study, miR-511 was found to be downregulated in GC and an inverse correlation was observed between TRIM24 and miR-511 expression in primary GC tissues and cell lines. Dual-luciferase reporter assay further verified TRIM24 is a direct target of miR-511. Functional assays showed miR-511 overexpression inhibited cell growth, colony formation ability and cell cycle progression. Conversely, inhibition of endogenous miR-511 promoted these phenotypes in GC cells. Moreover, reintroduction of TRIM24 rescued miR-511-induced inhibitory effects on GC cells. Furthermore, miR-511 elicits tumor-suppressive effects through inactivating PI3K/AKT and Wnt/β-catenin pathways by suppressing TRIM24.ConclusionsOur results provide the new evidence supporting the tumor-suppressive role of miR-511 in GC by suppressing TRIM24, suggesting that this novel miR-511/TRIM24 axis is critical in the control of gastric cancer tumorigenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-017-0489-1) contains supplementary material, which is available to authorized users.

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“…Apoptosis induced by parquet was associated with decreased PIK3R3 expression and caspase activation [28]. Furthermore, PIK3R3 could promote cell migration and invasion in various types of cancer via different mechanisms [29], for example, this protein could enhance the migration and invasion of colorectal cancer by SLUG triggered EMT [19]. Similar to above-mentioned results, our data demonstrated that PIK3R3 could promote the migration and invasion of PC cells for the first time by experiments both in vitro and in vivo , and this function of PIK3R3 might be depending on the ZEB1 induced EMT.…”

Section: Discussionmentioning

confidence: 99%

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

Peng

Zhu

Yin

et al. 2018

Cell Physiol Biochem

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Background/Aims: PIK3R3 is a regulatory subunit of phosphatidylinositol 3-kinase (PI3K) which plays an essential role in the metastasis of several types of cancer. However, whether PIK3R3 can promote the metastasis of pancreatic cancer (PC) is still unclear. In this study, we characterized the role of PIK3R3 in metastasis of PC and underlying potential mechanisms. Methods: RT-PCR, western blot, immunofluorescence (IF) and immunohistochemistry (IHC) were applied to investigate the expression of genes and proteins in different cell lines and tissues. To assess the function of PIK3R3 and related mechanisms, the cells with RNAi-mediated knockdown or overexpression were used to perform a series of in vitro and in vivo assays. Results: PIK3R3 was significantly overexpressed in pancreatic cancer tissues, especially in metastatic cancer tissues, as well as in pancreatic cancer cells. Functional assays suggested that overexpression or knockdown of PIK3R3 could respectively promote or suppress the migration and invasion of PC cells in vitro and in vivo. Further mechanism related studies demonstrated that ERK1/2-ZEB1 pathway-triggered epithelial-mesenchymal transition (EMT) might be responsible for the PIK3R3-induced PC cell migration and invasion. Conclusion: PIK3R3 could promote the metastasis of PC by facilitating ZEB1 induced EMT, and could act as a potential therapeutic target to limit PC metastasis.

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MiR-511 inhibits growth and metastasis of human hepatocellular carcinoma cells by targeting PIK3R3

Cited by 39 publications

References 31 publications

Lnc RNA ‐ PAGBC acts as a micro RNA sponge and promotes gallbladder tumorigenesis

Lnc RNA ‐ PAGBC acts as a micro RNA sponge and promotes gallbladder tumorigenesis

Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer

PIK3R3 Promotes Metastasis of Pancreatic Cancer via ZEB1 Induced Epithelial-Mesenchymal Transition

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