LncRNA‐LOC101928316 contributes to gastric cancer progression through regulating PI3K‐Akt‐mTOR signaling pathway

Li, Chengyun; Liang, Geyu; Yang, Sheng; Sui, Jing; Wu, Wenjuan; Xu, Siyi; Ye, Yancheng; Shen, Bo; Zhang, Xiaomei; Zhang, Yan

doi:10.1002/cam4.2165

Cited by 22 publications

(19 citation statements)

References 27 publications

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“…Recently, dysregulated lncRNAs have been presented to be implicated in the malignant progression of GC via affecting the PI3K/AKT/mTOR signaling pathway [ 39 ]. For example, lncRNA LOC101928316 facilitated the development of GC by modulating the PI3K/AKT/mTOR signaling pathway [ 12 ]; MALAT1/miR-183/SIRT1 axis contributed to the regulation of GC via PI3K/AKT/mTOR pathway [ 13 ] and lncRNA XLOC_006753 could induce cell proliferation, cell cycle, and metastasis but inhibit apoptosis in multidrug-resistant GC cells through promoting the PI3K/AKT/mTOR pathway [ 33 ]. NEAT1 has reported to activate the PI3K/AKT pathway to facilitate GC cell viability and migration [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Wang

et al. 2020

Open Medicine

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Long non-coding RNAs (lncRNAs) were reported to promote the development of gastric cancer (GC). Nuclear-enriched abundant transcript 1 (NEAT1) played a great role in diverse cancers, but the mechanism of NEAT1 in GC remains indistinct. NEAT1 and AKT1 were distinctly up-regulated and miR-1294 was down-regulated in GC tissues and cells. Cell proliferation and metastasis were refrained but apoptosis was promoted in GC cells after knockdown of NEAT1. NEAT1 negatively regulated miR-1294 expression, and the miR-1294 inhibitor reverted the si-NEAT1-induced effect on GC cells. NEAT1 modulated AKT1 expression through miR-1294, and the si-NEAT1-induced effect was relieved by AKT1. NEAT1 affected phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway via regulating miR-1294 and AKT1. NEAT1 could modulate cell proliferation, apoptosis, and metastasis in GC cells by regulating the PI3K/AKT/mTOR signaling pathway via the miR-1294/AKT1 axis, showing the great potential for NEAT1 as a valid biomarker in the progression and treatment of GC.

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Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Wang

et al. 2020

Open Medicine

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“…Gastric cancer (GC) is a prevalent malignancy and also one of the leading causes of cancer-generated death all around the world [1][2][3]. Like other carcinomas, GC is featured by infinite cell proliferation and tumor growth, which is attributed to the promotive influences of oncogenic regulators and the inhibitory influences of tumor-suppressive regulators [4][5][6]. In the current time, the main treatment methods for GC patients are surgical operation, chemotherapy and radiotherapy [7,8].…”

Section: Introductionmentioning

confidence: 99%

LBX2-AS1/miR-219a-2-3p/FUS/LBX2 positive feedback loop contributes to the proliferation of gastric cancer

Yang

Dong

et al. 2019

Gastric Cancer

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Background Long non-coding RNAs (lncRNAs) are increasingly investigated in numerous carcinomas containing gastric cancer (GC). The aim of our research is to inquire about the expression profile and role of LBX2-AS1 in GC. Methods The expressions of LBX2-AS1, miR-219a-2-3p, FUS and LBX2 were measured by qRT-PCR. Western blot evaluated FUS and LBX2 protein levels. Cell proliferation and apoptosis were, respectively, evaluated by CCK-8, colony formation, EdU, flow cytometry and TUNEL assays. FISH and subcellular fractionation assays examined the position of LBX2-AS1. The binding between genes were certified by RIP, RNA pull-down, ChIP and luciferase reporter assays. Pearson correlation analysis analyzed the association of genes. Kaplan-Meier method detected the relationship of LBX2-AS1 expression with overall survival. Results The up-regulation of LBX2-AS1 in GC tissues and cells was verified. Function assays proved that LBX2-AS1 down-regulation restricted the proliferation ability. Then, we unveiled the LBX2-AS1/miR-219a-2-3p/FUS axis. Additionally, LBX2-AS1 positively regulated LBX2 mRNA stability via FUS. LBX2 transcriptionally modulated LBX2-AS1. In the end, rescue and in vivo experiments validated the whole regulatory mechanism. Conclusion LBX2-AS1/miR-219a-2-3p/FUS/LBX2 positive feedback loop mainly affected the proliferation and apoptosis abilities of GC cells, offering novel therapeutic targets for the treatment of patients with GC. Keywords Gastric cancer (GC) • LBX2 antisense RNA 1 (LBX2-AS1) • miR-219a-2-3p • Fused in sarcoma (FUS) • Ladybird homeobox 2 (LBX2)

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“…For example, a study showed that LOC101928316 regulates the progression of GC via modulating PI3K-Akt-mTOR signaling pathway. 34 A novel lncRNA TUBA4B can inhibit GC growth through regulating miR-214/miR-216a/b-PTEN axis. 35 Research also reported that lncRNA SEMA3B-AS1 regulates the proliferation of hepatocellular carcinoma cells by regulating miR-718/PETN axis.…”

Section: Discussionmentioning

confidence: 99%

<p>The Down-Regulation of lncRNA PCAT18 Promotes the Progression of Gastric Cancer via MiR-107/PTEN/PI3K/AKT Signaling Pathway</p>

Chen

Zhao

Wang

et al. 2019

OTT

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Purpose: LncRNAs are important regulators in cancers. In this study, we investigated the role of lncRNA PCAT18 in gastric cancer (GC). Patients and Methods: The level of PCAT18 in GC tissues and cells was determined by qRT-PCR. The cellular behaviors of GC cells with knockdown or overexpression of PCAT18 were respectively detected by CCK-8 assays, colony formation assays, flow cytometry and Western blot. A GC mice model was established by subcutaneous injection of MGC-803 and HGC-27 cells with the knockdown or overexpression of PCAT18. The tumor size and weight were measured, and IHC was performed to determine ki-67 level. Predicted by bioinformatics software and confirmed by dual-luciferase reporter assay, PCAT18 was involved in miR-107/PTEN axis, thus, the expression of and relationship among PCAT18, miR-107 and PTEN pathway were explored in clinical cases and GC cell lines. Rescue assay was performed in GC cells by co-transfection with miR-107 mimic or PCAT18. The PTEN/ PI3K/AKT pathway was then detected by Western blot. Results: PCAT18 was down-regulated in GC tissues and cells, and it had a significant diagnostic value for GC. The expression of PCAT18 was highly associated with tumor size, and PCAT18 was found to inhibit GC growth in vitro and in vivo. It was also found that PCAT18 was involved in PTEN/PI3K/AKT signaling pathway through targeting miR-107. Conclusion: PCAT18 inhibits the progression of GC via miR-107/PTEN/PI3K/AKT signaling pathway. Additionally, PCAT18 is possibly a promising target for treatment of GC.

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LncRNA‐LOC101928316 contributes to gastric cancer progression through regulating PI3K‐Akt‐mTOR signaling pathway

Cited by 22 publications

References 27 publications

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

LBX2-AS1/miR-219a-2-3p/FUS/LBX2 positive feedback loop contributes to the proliferation of gastric cancer

<p>The Down-Regulation of lncRNA PCAT18 Promotes the Progression of Gastric Cancer via MiR-107/PTEN/PI3K/AKT Signaling Pathway</p>

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