lnCAR: A Comprehensive Resource for lncRNAs from Cancer Arrays

Zheng, Yueyuan; Xu, Qingxian; Liu, Mengni; Hu, Huanjing; Xie, Yubin; Zuo, Zhixiang

doi:10.1158/0008-5472.can-18-2169

Cited by 55 publications

(51 citation statements)

References 34 publications

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“…In the present study, the relevance of lncRNA expression levels to invasive breast carcinoma were based on RNA sequencing (RNA-Seq) data, while in some other databases, the cancer-related lncRNAs are identified using microarrays (45). For example, the lnCAR database extracts clinical information and gene expression microarray data from the GEO database (46). RNA-Seq and microarrays are two of the most common methods of transcript expression detection.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Yin

et al. 2020

Oncol Lett

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Breast cancer is one of the most common types of cancer among women worldwide and needs more sensitive prognostic biomarkers to improve its treatment. In the present study, differentially expressed long non-coding RNAs (lncRNAs) in invasive breast carcinoma from The Cancer Genome Atlas and cBioPortal database were investigated, identifying 292 differentially expressed lncRNAs in 1,100 cases. By analyzing the overall survival rate, 10 lncRNAs were significantly correlated with poor prognosis. To explore the underlying molecular mechanisms of the 10 prognosis-related lncRNAs, bioinformatic methods were used to predict the potential target miRNAs, mRNAs and proteins, and to construct a lncRNA-miRNA-mRNA regulatory network and lncRNA-protein interaction network. Finally, the functions of the target genes and proteins were insvestigated using Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analyses. The results showed that these 10 lncRNAs could be novel prognostic markers for invasive breast carcinoma and the present study aimed to provide novel insight into the diagnosis and treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Yin

et al. 2020

Oncol Lett

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“…Our results showed that the level of MSC-AS1 in GC tissue samples was significantly higher than that in the tumor-adjacent tissue samples (P<0.0001, Figure 1A). Moreover, TCGA data from the gene expression profiling interactive analysis (GEPIA) platform [24] and gene expression omnibus (GEO) datasets (GSE54129, GSE65801, and GSE13911) from lnCAR platform [25] consistently revealed the upregulated expression of MSC-AS1 in GC tissues compared to normal tissues (P<0.05, Figure 1B and Supplementary Figure 1). MSC-AS1 expressed at higher levels in GC cells (MKN-45, AGS, SGC-7901, and MGC-803) as compared with normal GES-1 gastric mucosal cells (P<0.05, Figure 1C).…”

Section: The Elevated Level Msc-as1 Associated With the Poor Prognosimentioning

confidence: 96%

Long non-coding RNA MSC-AS1 facilitates the proliferation and glycolysis of gastric cancer cells by regulating PFKFB3 expression

Jin¹,

Qiao²,

Fan³

et al. 2021

Int. J. Med. Sci.

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Long non-coding RNA musculin antisense RNA 1 (lncRNA MSC-AS1) has been recognized as an oncogene in pancreatic cancer, hepatocellular carcinoma, nasopharyngeal carcinoma, and renal cell carcinoma. However, the functional significance of MSC-AS1 and its underlying mechanism in gastric cancer (GC) progression remain unclear. In this study, we demonstrated that the expression of MSC-AS1 in GC tissues was significantly higher than that in non-tumor tissues. Moreover, the elevated level of MSC-AS1 was detected in GC cells (MKN-45, AGS, SGC-7901, and MGC-803) compared to normal GES-1 gastric mucosal cells. The cancer genome atlas (TCGA) data further indicated that the high level of MSC-AS1 was closely correlated with advanced tumor stage and poor prognosis of GC. Next, we revealed that MSC-AS1 knockdown inhibited the proliferation, glucose consumption, lactate production, and pyruvate production of MGC-803 cells. Conversely, MSC-AS1 overexpression enhanced the proliferation and glycolysis of AGC cells. Mechanistically, modulating MSC-AS1 level affected the expression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), but did not impact the levels of hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2) in GC cells. Based on this, we reversed the MSC-AS1 knockdown-induced the inhibition of cell proliferation and glycolysis by restoring PFKFB3 expression in MGC-803 cells. In conclusion, MSC-AS1 facilitated the proliferation and glycolysis of GC cells by maintaining PFKFB3 expression.

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“…According to the lnCAR (https://lncar.renlab.org/) website [30], miR-27b-3p, which was previously reported to be a tumor suppressor in DLBCL, was predicted as a candidate target of HCP5 ( Figure 4A). We then revealed that HCP5 knockdown significantly increased the level of miR-27b-3p in OCI-LY3 and OCI-LY7 cells (P<0.05, Figure 4B).…”

Section: Mir-27b-5p Is a Direct Target Of Hcp5mentioning

confidence: 99%

Geniposide inhibits proliferation and induces apoptosis of diffuse large B-cell lymphoma cells by inactivating the HCP5/miR-27b-3p/MET axis

Hu¹,

Zhao²,

Liu³

et al. 2020

Int. J. Med. Sci.

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Diffuse large B-cell lymphoma (DLBCL) is commonly treated with R-CHOP, but ~30 to 50% of the patients are poorly responsive to this strategy. Geniposide, an extract from the Gardenia jasminoides Ellis, plays antitumor roles in human gastric cancer, hepatocellular carcinoma, and oral squamous carcinoma. However, the effects of geniposide treatment on DLBCL cells, as well as its underlying mechanism, are still unknown. Here, we found that geniposide inhibited the proliferation of OCI-LY7 and OCI-LY3 cells in a dose-dependent manner. Furthermore, geniposide increased the percentage of apoptotic cells and upregulated the levels of cleaved PARP and cleaved caspase-3 in DLBCL cells. Interestingly, geniposide treatment significantly reduced the expression of the long noncoding RNA HLA complex P5 (lncRNA HCP5) in DLBCL cells. HCP5 expression was revealed to be upregulated in DLBCL tissues and cell lines. Moreover, HCP5 knockdown resulted in proliferation inhibition and apoptosis in OCI-LY7 and OCI-LY3 cells. miR-27b-3p was predicted as a potential target of HCP5 using the lnCAR web tool. Both HCP5 silencing and geniposide treatment increased the level of miR-27b-3p in DLBCL cells. Accordingly, a luciferase reporter assay identified miR-27b-3p as a direct target of HCP5. The expression of miR-27b-3p was upregulated and inversely correlated with the HCP5 level in DLBCL tissues. HCP5 knockdown reduced MET protein expression, which was subsequently rescued by miR-27b-3p silencing in DLBCL cells. Importantly, the restoration of MET partially reversed the geniposide-induced proliferation inhibition and apoptosis of DLBCL cells. In conclusion, geniposide inhibits the proliferation and induces the apoptosis of DLBCL cells at least partially by regulating the HCP5/miR-27b-3p/MET axis, indicating a potential strategy for DLBCL treatment.

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lnCAR: A Comprehensive Resource for lncRNAs from Cancer Arrays

Cited by 55 publications

References 34 publications

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Bioinformatics analysis of prognosis-related long non-coding RNAs in invasive breast carcinoma

Long non-coding RNA MSC-AS1 facilitates the proliferation and glycolysis of gastric cancer cells by regulating PFKFB3 expression

Geniposide inhibits proliferation and induces apoptosis of diffuse large B-cell lymphoma cells by inactivating the HCP5/miR-27b-3p/MET axis

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