LINC00514 promotes gastric cancer cell growth and EMT progression via miR-204-3p/KRAS

Yuan, Ling; Li, Jiaxin; Yang, Yi; Chen, Yan; Yang, Baofeng; Ye, Mengyi; Mao, Xiongjie; Ma, Tingting; Yu, Lei; Yang, Nan

doi:10.18632/aging.202905

Cited by 12 publications

(11 citation statements)

References 37 publications

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“…Tumor cells have higher motility and aggressiveness after EMT, in which the reduction of epithelial markers such as E-cadherin and the increase of mesenchymal markers such as N-cadherin are essential hallmarks of this process [ 39 ]. The present study confirmed that after LINC00514 knockdown, E-cadherin was upregulated; conversely, N-cadherin was decreased, suggesting that LINC00514 might have a regulatory role in the EMT of NSCLC, and a similar effect has been reported in gastric cancer [ 40 ]. Wnt/β-catenin also serves as a common upstream signal for EMT, and an aberrant Wnt signaling in NSCLC, which often induces cellular EMT [ 41 ].…”

Section: Discussionsupporting

confidence: 88%

LINC00514 facilitates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in non-small cell lung cancer by acting on the Wnt/β-catenin signaling pathway

Zhu

Yang

et al. 2022

Bioengineered

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The long non-coding RNA (lncRNA) LINC00514 was identified to play an essential oncogenic function in different human cancers, but its effects in non-small cell lung cancer (NSCLC) are yet to be elucidated. In this study, we evaluated the function of LINC00514 in NSCLC. LINC00514 expression and prognosis in NSCLC were analyzed using qRT-PCR and online bioinformatic tools. The bioeffects of LINC0514 in NSCLC cells were examined using cell counting kit-8, colony formation, and transwell assays. Western blotting was used to measure the expression of the target proteins. The LINC00514 regulation of the Wnt/β-catenin signaling pathway was assessed using a specific agonist (LiCl) and luciferase reporter assay. We found that LINC00514 expression was elevated in NSCLC cells and clinical samples and that increased LINC00514 expression predicted poorer patient prognosis. Silencing LINC00514 suppresses proliferation, migration, and invasion of NSCLC cells. Downregulation of LINC00514 inhibited Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT). Moreover, suppression of the biological phenotypes of NSCLC cells induced by LINC00514 gene silencing was restored after LiCl treatment. Finally, we found that silencing LINC00514 attenuated the growth of xenograft tumors in vivo. Altogether, this study provides the latest convincing evidence that LINC00514 facilitates the malignant biological behavior of NSCLC cells through activation of the Wnt/β-catenin pathway, which might offer a beneficial approach for the treatment of NSCLC.

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Section: Discussionsupporting

confidence: 88%

LINC00514 facilitates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in non-small cell lung cancer by acting on the Wnt/β-catenin signaling pathway

Zhu

Yang

et al. 2022

Bioengineered

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“…The loss of epithelial characteristics and the acquisition of mesenchymal features reduce cell adhesion and increase cell mobility. In addition, our previous experiments also showed that LINC00514 was up-regulated in GC specimens compared with non-tumor specimens, and overexpression of LINC00514 induced GC cell growth and EMT progression[ 26 ]. We used immunodeficient nude mice for tumor-forming experiments in vivo .…”

Section: Discussionmentioning

confidence: 99%

18β-glycyrrhetinic acid regulates mitochondrial ribosomal protein L35-associated apoptosis signaling pathways to inhibit proliferation of gastric carcinoma cells

Yuan¹,

Yang²,

Li³

et al. 2022

WJG

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BACKGROUND Gastric carcinoma (GC) is a common gastrointestinal malignancy worldwide. Based on the cancer-related mortality, the current prevention and treatment strategies for GC still show poor clinical results. Therefore, it is important to find effective drug treatment targets. AIM To explore the mechanism by which 18β-glycyrrhetinic acid (18β-GRA) regulates mitochondrial ribosomal protein L35 (MRPL35) related signal proteins to inhibit the proliferation of GC cells. METHODS Cell counting kit-8 assay was used to detect the effects of 18β-GRA on the survival rate of human normal gastric mucosal cell line GES-1 and the proliferation of GC cell lines MGC80-3 and BGC-823. The apoptosis and cell cycle were assessed by flow cytometry. Cell invasion and migration were evaluated by Transwell assay, and cell scratch test was used to detect cell migration. Furthermore, a tumor model was established by hypodermic injection of 2.5 × 10 6 BGC-823 cells at the selected positions of BALB/c nude mice to determine the effect of 18β-GRA on GC cell proliferation, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect MRPL35 expression in the engrafted tumors in mice. We used the term tandem mass tag (TMT) labeling combined with liquid chromatography–tandem mass spectrometry to screen for differentially expressed proteins (DEPs) extracted from GC cells and control cells after 18β-GRA intervention. A detailed bioinformatics analysis of these DEPs was performed, including Gene Ontology annotation and enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, and so on. Moreover, STRING database ( ) was used to predict protein-protein interaction (PPI) relationships and Western blot was used to detect the expression of proteins of interest in GC cells. RESULTS The results indicated that 18β-GRA could inhibit the proliferation of GC cells in a dose- and time-dependent manner. It could induce GC cell apoptosis and arrest the cell cycle at G0/G1 phase. The proportion of cells arrested at S phase decreased with the increase of 18-GRA dose, and the migration and invasiveness of GC cells were inhibited. The results of animal experiments showed that 18β-GRA could inhibit tumor formation in BALB/c nude mice, and qRT-PCR results showed that MRPL35 expression level was significantly reduced in the engrafted tumors in mice. Using TMT technology, 609 DEPs, among which 335 were up-regulated and 274 were down-regulated, were identified in 18β-GRA intervention compared with control. We found that the intervention of 18β-GRA in GC cells involved many important biological processes and signaling pathways, such as cellular processes, biological regulation, and TP53 signaling pathway. Notably, after the drug intervention, MRPL35 expression was significantly down-regulated ( ...

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“…Research on competing endogenous RNA (ceRNA) networks that regulate EMT‐related pathways in patients with GC has recently emerged. Table 2 provides the complete ceRNA control axis of EMT in Correa's cascade 119‐138 . The occurrence of EMT is linked to changes in microbiota through various mechanisms, particularly the changes in the abundance of H. pylori .…”

Section: Characteristics and Predictive Value Of H Pylori In Correa's...mentioning

confidence: 99%

“…Table 2 provides the complete ceRNA control axis of EMT in Correa's cascade. [119][120][121][122][123][124][125][126][127][128][129][130][131][132][133][134][135][136][137][138] The occurrence of EMT is linked to changes in microbiota through various mechanisms, particularly the changes in the abundance of H. pylori. This network may provide a theoretical basis for gastric microbiota-associated EMT therapy in Correa's cascade.…”

Section: Gastric Microbiota Composition At Different Stages Of Correa...mentioning

confidence: 99%

Dynamic variations of the gastric microbiota: Key therapeutic points in the reversal of Correa's cascade

Zhang

et al. 2022

Intl Journal of Cancer

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Correa's cascade is a dynamic process in the development of intestinal-type gastric cancer (GC), and its pathological features, gastric microbiota and interactions between microorganisms and their hosts vary at different developmental stages.The characteristics of cells, tissues and gastric microbiota before or after key therapeutic points are critical for monitoring malignant transformation and early tumour reversal. This review summarises the pathological features of gastric mucosa, characteristics of gastric microbiota, specific microbial markers, microbe-microbe interactions and microbe-host interactions at different stages in Correa's cascade. The markers related to each Correa's cascade point were analysed in detail. We attempted to identify key therapeutic points for early cancer reversal and provide a novel approach to reduce the incidence of GC and improve precise treatment.

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LINC00514 promotes gastric cancer cell growth and EMT progression via miR-204-3p/KRAS

Cited by 12 publications

References 37 publications

LINC00514 facilitates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in non-small cell lung cancer by acting on the Wnt/β-catenin signaling pathway

LINC00514 facilitates cell proliferation, migration, invasion, and epithelial-mesenchymal transition in non-small cell lung cancer by acting on the Wnt/β-catenin signaling pathway

18β-glycyrrhetinic acid regulates mitochondrial ribosomal protein L35-associated apoptosis signaling pathways to inhibit proliferation of gastric carcinoma cells

Dynamic variations of the gastric microbiota: Key therapeutic points in the reversal of Correa's cascade

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