Pseudogene PLGLA exerts anti-tumor effects on hepatocellular carcinoma through modulating miR-324-3p/GLYATL1 axis.
TLDR
In this paper, the role of Plasminogen like A (PLGLA) in hepatocellular carcinoma (HCC) was explored using The Cancer Genome Atlas (TCGA) datasets.About:
This article is published in Digestive and Liver Disease.The article was published on 2021-11-12 and is currently open access. It has received 5 citations till now. The article focuses on the topics: Competing endogenous RNA & Cancer research.read more
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microRNA-324-3p suppresses the aggressive ovarian cancer by targeting WNK2/RAS pathway
TL;DR: It is demonstrated that miR-324-3p suppressed ovarian cancer progression by targeting the WNK2/RAS pathway and provides theoretical evidence for the clinical application potential of miR+3p.
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NAPSB as a predictive marker for prognosis and therapy associated with an immuno-hot tumor microenvironment in hepatocellular carcinoma
Yu-Mei Ning,Kun-Ju Lin,Xiao-Ping Liu,Yan Ding,Xiang Jiang,Zhang Zhang,Yu-Ting Xuan,Li-Wei Dong,Lan Liu,Fan Wang,Qiu-Jie Zhao,Haizhou Wang,Jun Fang +12 more
TL;DR: Napsin B Aspartic Peptidase, Pseudogene (NAPSB) was associated with CD4 + T cell infiltration in pancreatic ductal adenocarcinoma as discussed by the authors .
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Establishing a prognostic model of chromatin modulators and identifying potential drug candidates in renal clear cell patients
TL;DR: In this paper , the functional and prognostic value of chromatin regulators in renal carcinoma patients was investigated using univariate Cox regression analysis and LASSO regression analysis to construct a risk model for predicting the prognosis of renal cancer.
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Establishing a prognostic model of chromatin modulators and identifying potential drug candidates in renal clear cell patients Introduction
TL;DR: Wang et al. as mentioned in this paper used univariate Cox regression analysis and LASSO regression analysis to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer.
Posted ContentDOI
Establishing a prognostic model of chromatin modulators and identifying potential drug candidates in renal clear cell patients Introduction
TL;DR: Wang et al. as mentioned in this paper used univariate Cox regression analysis and LASSO regression analysis to select prognostic chromatin-regulated genes and use them to construct a risk model for predicting the prognosis of renal cancer.
References
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The biology of Hepatocellular carcinoma: implications for genomic and immune therapies
TL;DR: Alterations in the TERT promoter, as well as in TP53 and the cell cycle machinery, and in the PI3K/Akt/mTor axis, aswell as aberrant angiogenesis and epigenetic anomalies, appear to be major events in HCC.
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Epithelial Mesenchymal and Endothelial Mesenchymal Transitions in Hepatocellular Carcinoma: A Review.
TL;DR: The metastatic pathway of HCC seems to be related to the Wnt- or, rather, TGFβ1-mediated inflammation-angiogenesis-EMT-CSCs crosstalk link, and molecular therapy should target this molecular axis controlling the HCC microenvironment.
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miR-324-3p promotes gastric cancer development by activating Smad4-mediated Wnt/beta-catenin signaling pathway.
Guangli Sun,Zheng Li,Weizhi Wang,Zheng Chen,Lei Zhang,Qing Li,Song Wei,Bowen Li,Jianghao Xu,Liang Chen,Zhongyuan He,Kai Ying,Xuan Zhang,Hao Xu,Diancai Zhang,Zekuan Xu +15 more
TL;DR: The results suggested that miR-324-3p promoted GC through activating the Smad4-mediated Wnt/beta-catenin signaling pathway and may be a potential therapeutic target to prevent GC progression.
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LINC00261 suppresses human colon cancer progression via sponging miR-324-3p and inactivating the Wnt/β-catenin pathway.
TL;DR: Overall, the results showed that LINC00261 repressed colon cancer progression via regulating miR‐324‐3p and the Wnt pathway, and could be established as a novel therapeutic target for colon cancer.
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LncRNA NBR2 inhibits tumorigenesis by regulating autophagy in hepatocellular carcinoma.
TL;DR: The data indicated that NBR2 served as a tumor suppressor gene in hepatocellular carcinoma and suppressed autophagy-induced cell proliferation at least partly through ERK and JNK pathways.