The CAGE–MiR-181b-5p–S1PR1 Axis Regulates Anticancer Drug Resistance and Autophagy in Gastric Cancer Cells

Yeon, Minjeong; Kim, Youngmi; Pathak, Deepak; Kwon, Eunju; Kim, Dong Young; Jeong, Myeong Seon; Jung, Hyun Suk; Jeoung, Dooil

doi:10.3389/fcell.2021.666387

Cited by 28 publications

(38 citation statements)

References 43 publications

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“…Several studies have already reported the activation of diverse biological processes via experimental results or bioinformatic analysis. Yeon et al 6 reported that the miR-181b-5p/CAGE/S1PR1 axis can alter autophagic flux, resulting in enhanced sensitivity to anticancer drugs. Wang et al 7 revealed that cisplatin resistance was transmitted by the exosomal lncRNA HOTTIP, which targets the miR-218/HMGA1 axis in cisplatin-sensitive cells.…”

Section: Introductionmentioning

confidence: 99%

Extracellular Matrix-Associated Pathways Promote the Progression of Gastric Cancer by Impacting the Dendritic Cell Axis

Wang¹,

Wang²,

Hu³

et al. 2021

IJGM

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Background: Gastric cancer (GC) is the third most frequent malignant tumour in the Chinese population, let alone the whole world. Recently, most prognostic models have only focused on the levels of several genes, miRNAs, lncRNAs, gene mutations, or DNA methylation; however, the activation status of biological pathways is more stable and can reflect the comprehensive inner conditions of tumours. Methods: We collected samples from the Cancer Genome Atlas Stomach Adenocarcinoma (TCGA-STAD) cohort and GSE62254 cohort, with a total of 594 patients. We employed GSEA to first compare the diverse activated signalling pathways between dead GC patients and living patients. The least absolute shrinkage and selection operator (LASSO) regression analysis was subsequently performed by the "glmnet" package to generate a prognostic signature.Results: We extracted a total of 218 genes from the KEGG Focal Adhesion and KEGG ECM Receptor Interaction pathways, which showed significant activation in dead GC patients in two enrolled cohorts, for subsequent LASSO analysis. In the TCGA-STAD cohort, patients in the high-risk group faced a significantly poorer prognosis than those in the low-risk group (P < 0.001, HR: 4.62, 95% CI: 3.447-6.183), with an AUC of 0.694. In the GSE62254 cohort, the HR value was 4.94 (95% CI: 3.413-7.165), and the AUC value was as high as 0.834. A high-risk score and poor prognosis correlated with infiltrated dendritic cells, and the receptor of IFN-α was also positively linked with the risk score, as well as poor prognosis. GC patients with high-risk scores were more likely to respond to CTLA4 treatment but not PD1 treatment. Conclusion: Taken together, we established and verified an extracellular matrix prognostic model of gastric cancer patients. The model can be used to evaluate the risk of death of GC patients, as well as the response to anti-CTLA4 immunotherapy.

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Section: Introductionmentioning

confidence: 99%

Extracellular Matrix-Associated Pathways Promote the Progression of Gastric Cancer by Impacting the Dendritic Cell Axis

Wang¹,

Wang²,

Hu³

et al. 2021

IJGM

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“…Then, we further investigated the possible mechanism underlying the regulative effect of FEZF1-AS1 on chemoresistance of GC cells. Several previous studies had reported that enhanced autophagy is one of the important mechanisms of increased chemo-resistance in several tumor cells including GC cells ( Yuan et al, 2016 ; Pei et al, 2018 ; Yeon et al, 2021 ). Therefore, we hypothesized that FEZF1-AS1 can regulate chemoresistance in GC cells via modulating autophagy.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FEZF1-AS1 Promotes Multi-Drug Resistance of Gastric Cancer Cells via Upregulating ATG5

Gui

Zhao

Sun

et al. 2021

Front. Cell Dev. Biol.

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Long non-coding RNAs (lncRNAs) play important roles in human cancers including gastric cancer (GC). Dysregulation of lncRNAs is involved in a variety of pathological activities associated with gastric cancer progression and chemo-resistance. However, the role and molecular mechanisms of FEZF1-AS1 in chemoresistance of GC remain unknown. In this study, we aimed to determine the role of FEZF1-AS1 in chemoresistance of GC. The level of FEZF1-AS1 in GC tissues and GC cell lines was assessed by qRT-PCR. Our results showed that the expression of FEZF1-AS1 was higher in gastric cancer tissues than in adjacent normal tissues. Multivariate analysis identified that high level of FEZF1-AS1 is an independent predictor for poor overall survival. Increased FEZF1-AS1 expression promoted gastric cancer cell proliferation in vitro. Additionally, FEZF1-AS1 was upregulated in chemo-resistant GC tissues. The regulatory effect of FEZF1-AS1 on multi-drug resistance (MDR) in GC cells and the underlying mechanism was investigated. It was found that increased FEZF1-AS1 expression promoted chemo-resistance of GC cells. Molecular interactions were determined by RNA immunoprecipitation (RIP) and the results showed that FEZF1-AS1 regulated chemo-resistance of GC cells through modulating autophagy by directly targeting ATG5. The proliferation and autophagy of GC cells promoted by overexpression of LncFEZF1-AS1 was suppressed when ATG5 was knocked down. Moreover, knockdown of FEZF1-AS1 inhibited tumor growth and increased 5-FU sensitivity in GC cells in vivo. Taken together, this study revealed that the FEZF1-AS1/ATG5 axis regulates MDR of GC cells via modulating autophagy.

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“…Cancer cells may induce autophagy for survival in response to anti-cancer drugs [ 100 , 101 ]. Autophagy is positively associated with anti-cancer drug resistance [ 102 , 103 ]. The activation of phosphoinositide 3 (PI3K)/Akt signaling promoted autophagy and chemotherapy resistance in breast cancer cells [ 104 ].…”

Section: Role Of the Mir-200 Family In Anti-cancer Drug Resistancementioning

confidence: 99%

Potential of the miR-200 Family as a Target for Developing Anti-Cancer Therapeutics

Shim

Jeoung

2022

IJMS

Self Cite

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MicroRNAs (miRNAs) are small non-coding RNAs (18–24 nucleotides) that play significant roles in cell proliferation, development, invasion, cancer development, cancer progression, and anti-cancer drug resistance. miRNAs target multiple genes and play diverse roles. miRNAs can bind to the 3′UTR of target genes and inhibit translation or promote the degradation of target genes. miR-200 family miRNAs mostly act as tumor suppressors and are commonly decreased in cancer. The miR-200 family has been reported as a valuable diagnostic and prognostic marker. This review discusses the clinical value of the miR-200 family, focusing on the role of the miR-200 family in the development of cancer and anti-cancer drug resistance. This review also provides an overview of the factors that regulate the expression of the miR-200 family, targets of miR-200 family miRNAs, and the mechanism of anti-cancer drug resistance regulated by the miR-200 family.

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The CAGE–MiR-181b-5p–S1PR1 Axis Regulates Anticancer Drug Resistance and Autophagy in Gastric Cancer Cells

Cited by 28 publications

References 43 publications

Extracellular Matrix-Associated Pathways Promote the Progression of Gastric Cancer by Impacting the Dendritic Cell Axis

Extracellular Matrix-Associated Pathways Promote the Progression of Gastric Cancer by Impacting the Dendritic Cell Axis

LncRNA FEZF1-AS1 Promotes Multi-Drug Resistance of Gastric Cancer Cells via Upregulating ATG5

Potential of the miR-200 Family as a Target for Developing Anti-Cancer Therapeutics

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