CircMRPS35 suppresses gastric cancer progression via recruiting KAT7 to govern histone modification

Jie, Meng-Meng; Wu, Yaran; Gao, Mengyuan; Li, Xinzhe; Liu, Cheng; Ouyang, Qin; Tang, Qingyun; Shan, Changyu; Lv, Yang‐Fan; Zhang, Kebin; Dai, Qian; Chen, Yang; Zeng, Shuo; Li, Chenglin; Wang, Liting; He, Fengtian; Hu, C.; Yang, Shi‐Ming

doi:10.1186/s12943-020-01160-2

Cited by 118 publications

(91 citation statements)

References 44 publications

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“…ChIRP assay was implemented in HGC-27/MSC-exo and AGS/MSC-exo cells in line with the previous protocol 27 . All probes were synthesized with BiotinTEG at the 3' end.…”

Section: Chromatin Isolation By Rna Purification (Chirp) Assaymentioning

confidence: 99%

Exosome-transferred LINC01559 promotes the progression of gastric cancer via PI3K/AKT signaling pathway

Wang

et al. 2020

Cell Death Dis

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Increasing evidence indicates that long non-coding RNAs (lncRNAs) are associated with the progression of human cancers. However, the expression level and function of LINC01559 (long intergenic non-protein coding RNA 1559) in gastric cancer (GC) are rarely reported. Here we found that LINC01559 was upregulated in GC tissues based on GEPIA (Gene Expression Profiling Interactive Analysis) and TCGA (The Cancer Genome Atlas) databases. Also, LINC01559 was expressed at a lower level in GC cells than in mesenchymal stem cells (MSCs). In vitro experiments revealed that silencing LINC01559 remarkably hindered GC cell proliferation, migration and stemness. Then, we identified that LINC01559 was transmitted form MSCs to GC cells via the exosomes. Immunofluorescence staining and electron microscope validated the existence of exosomes in GC cells. Mechanistically, LINC01559 sponged miR-1343-3p to upregulate PGK1 (phosphoglycerate kinase 1), therefore activating PI3K/AKT pathway. Moreover, LINC01559 recruited EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to PTEN (phosphatase and tensin homolog) promoter, inducing the methylation of PTEN promoter and finally resulting in PTEN repression. Of note, LINC01559 targeted both PGK1 and PTEN to promote GC progression by activating PI3K/AKT pathway. Taken together, our study demonstrated that LINC01559 accelerated GC progression via upregulating PGK1 and downregulating PTEN to trigger phosphatidylinositol 3-kinase/AKT serine/threonine kinase (PI3K/AKT) pathway, indicating LINC01559 as a potential biomarker for GC treatment.

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“…ChIRP assay was implemented in HGC-27/MSC-exo and AGS/MSC-exo cells in line with the previous protocol 27 . All probes were synthesized with BiotinTEG at the 3' end.…”

Section: Chromatin Isolation By Rna Purification (Chirp) Assaymentioning

confidence: 99%

Exosome-transferred LINC01559 promotes the progression of gastric cancer via PI3K/AKT signaling pathway

Wang

et al. 2020

Cell Death Dis

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“…9,10 CircRNA is considered to be an important regulator of cancer progression and mainly plays anti-cancer or pro-cancer role. 11,12 At present, many circRNAs are found in NSCLC, and their functions are illuminated. For instance, hsa_circ_0011780 has been proved to be an anti-cancer circRNA of NSCLC, which can inhibit the proliferation and metastasis of NSCLC cells.…”

Section: Introductionmentioning

confidence: 99%

<p>Circ_0000376, a Novel circRNA, Promotes the Progression of Non-Small Cell Lung Cancer Through Regulating the miR-1182/NOVA2 Network</p>

Li¹,

Long²,

Niu³

et al. 2020

CMAR

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Background: Hypoxia has been shown to induce the malignant progression of cancer, including non-small cell lung cancer (NSCLC). Circular RNA (circRNA) is considered to be an important regulator of cancer progression. However, the role of a newly discovered circRNA, circ_0000376, in the progression of NSCLC is unclear. Methods: The relative expression levels of circ_0000376, miR-1182 and neuro-oncological ventral antigen 2 (NOVA2) were detected via quantitative real-time polymerase chain reaction (qRT-PCR). Glucose consumption and lactate production were determined using Glucose Assay Kit and Lactate Assay Kit, respectively. Moreover, the protein levels of glycolysis markers and NOVA2 were measured using Western blot (WB) analysis. Furthermore, 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to assess cell viability, and transwell assay was employed to evaluate cell migration and invasion. The interaction between miR-1182 and circ_0000376 or NOVA2 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. In addition, animal experiments were conducted to assess the influence of circ_0000376 silencing on NSCLC tumor growth in vivo. Results: Circ_0000376 was upregulated in NSCLC, and its high expression was related to the poor overall survival of NSCLC patients. Hypoxia could enhance circ_0000376 expression and promote the glycolysis, viability, migration, and invasion of NSCLC cells. However, silencing of circ_0000376 could inhibit the glycolysis, viability, migration, and invasion of hypoxia-induced NSCLC cells. Additionally, circ_0000376 could sponge miR-1182, and miR-1182 could target NOVA2. MiR-1182 silencing could reverse the inhibitory effect of circ_0000376 knockdown on NSCLC progression, and NOVA2 overexpression also could reverse the suppressive effect of miR-1182 overexpression on NSCLC progression. Meanwhile, miR-1182 inhibitor could invert the negative regulation effect of circ_0000376 silencing on NOVA2 expression. In addition, circ_0000376 knockdown inhibited the NSCLC tumor growth via regulating the miR-1182 and NOVA2 expression in vivo. Conclusion: Circ_0000376 promoted NSCLC progression by regulating the miR-1182/NOVA2 axis, suggesting that circ_0000376 might be a potential biomarker for NSCLC treatment.

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“…As circRNA has the characteristics of stability and tissue specificity, thus it may become a tumor marker and be involved in progression of gastric cancer. Present study shows that Circ_0032821 promotes gastric cancer development by activating the MEK1/ ERK1/ 2; CircMRPS35 inhibits the progression of gastric cancer; Silencing RACRACGAP1 can enhance the sensitivity to Apatinib by targeting miR‐3657; CircRNA_0005075 inhibits gastric cancer growth via miR‐431/ p53/ epithelial stromal transformation axis; circ_0006282 promotes gastric cancer growth through miR‐155/ FBXO22 axis 11‐15 …”

Section: Discussionmentioning

confidence: 72%

hsa_circ_0000520 influences herceptin resistance in gastric cancer cells through PI3K‐Akt signaling pathway

Wang

et al. 2020

Clinical Laboratory Analysis

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Background To investigate whether hsa_circ_0000520 affects Herceptin resistance in gastric cancer by regulating the PI3K‐AKT signaling. Methods The expression of hsa_circ_0000520 was detected by qRT‐PCR in gastric cancer tissues and cell lines. A Herceptin‐resistant gastric cancer cell was established. PcDNA and pcDNA‐hsa_circ_0000520 were transfected into NCI‐N87R cells and treated with Herceptin at a concentration of 10 μg/mL for 24 hours. MTT tested cell proliferation, and apoptosis was measured by flow cytometry. IGF‐1 treatment was used to activate PI3K‐Akt signaling. The expression levels of related proteins were detected. Results The expression of hsa_circ_0000520 was reduced in gastric cancer tissues and cell lines, and hsa_circ_0000520 in NCI‐N87R cells was significantly lower than that of NCI‐N87 cells. Compared with the CON group, the cell viability of the Herceptin group was significantly reduced, the apoptosis rate was significantly increased, the level of Bax protein was significantly increased, and the levels of Bcl‐2, p‐PI3K, and p‐Akt protein were significantly reduced. Compared with the Herceptin + pcDNA group, the cell viability of the Herceptin + hsa_circ_0000520 group was significantly reduced, the apoptosis rate was significantly increased, the level of Bax protein was significantly increased, and the levels of p‐PI3K and p‐Akt proteins were significantly reduced. After IGF‐1 treatment, the cell viability was significantly increased, the apoptosis rate was significantly reduced, the level of Bax protein was significantly reduced, and the level of Bcl‐2 protein was significantly increased. Conclusion Hsa_circ_0000520 overexpression may reverse the Herceptin resistance of gastric cancer cells by inhibiting the PI3K‐Akt signaling pathway.

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CircMRPS35 suppresses gastric cancer progression via recruiting KAT7 to govern histone modification

Cited by 118 publications

References 44 publications

Exosome-transferred LINC01559 promotes the progression of gastric cancer via PI3K/AKT signaling pathway

Exosome-transferred LINC01559 promotes the progression of gastric cancer via PI3K/AKT signaling pathway

<p>Circ_0000376, a Novel circRNA, Promotes the Progression of Non-Small Cell Lung Cancer Through Regulating the miR-1182/NOVA2 Network</p>

hsa_circ_0000520 influences herceptin resistance in gastric cancer cells through PI3K‐Akt signaling pathway

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