Long non-coding RNA PTPRG-AS1/microRNA-124-3p regulates radiosensitivity of nasopharyngeal carcinoma via the LIM Homeobox 2-dependent Notch pathway through competitive endogenous RNA mechanism

Shen, Zhangquan; Wu, Yang Chang; He, Guansheng

doi:10.1080/21655979.2022.2037364

Cited by 10 publications

(11 citation statements)

References 38 publications

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“…The Gene Expression Omnibus (GEO) database was used to identify lncRNAs with abnormally high PTPRG-AS1 expression. LncRNA PTPRG-AS1 promotes radiosensitivity of NPC cells as a ceRNA [ 51 ]. LncRNA PTPRG-AS1 adsorbs miR-194-3p and miR-124-3p negatively regulate PRC1 and LHX2, respectively [ 50 , 51 ].…”

Section: Biological Functions Of Lncrna/circrna-mediated Cerna Networ...mentioning

confidence: 99%

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Insight into LncRNA- and CircRNA-Mediated CeRNAs: Regulatory Network and Implications in Nasopharyngeal Carcinoma—A Narrative Literature Review

Zhang

Xin

et al. 2022

Cancers

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Nasopharyngeal carcinoma (NPC) is a kind of head-and-neck malignant tumor, and distant metastasis treatment resistance is the leading cause of patient death. In-depth understanding of NPC progression and treatment failure remains to be explored. Long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) are noncoding RNAs that play key regulatory role in shaping tumor cell activities. Recent studies have revealed that lncRNA and circRNA function as competitive endogenous RNAs (ceRNAs) by regulating the posttranscriptional expression of genes as miRNA baits. The imbalanced ceRNA networks derived from lncRNA/circRNA-miRNA-mRNA interaction are widely found to contribute to NPC development. Herein, we summarize typical examples of lncRNA/circRNA-associated ceRNAs in recent years, which involved the potential molecular mechanisms in the regulation of proliferation, apoptosis, treatment resistance and metastasis of NPC, and discuss their potential clinical significance in the prognosis and treatment of NPC. Interpreting the involvement of ceRNAs networks will provide new insight into the pathogenesis and treatment strategies of NPC. However, ceRNA regulatory mechanism has some limitations currently. Screening the most effective ceRNA targets and the clinical application of ceRNA still has many challenges.

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Section: Biological Functions Of Lncrna/circrna-mediated Cerna Networ...mentioning

confidence: 99%

“…LncRNA PTPRG-AS1 promotes radiosensitivity of NPC cells as a ceRNA [ 51 ]. LncRNA PTPRG-AS1 adsorbs miR-194-3p and miR-124-3p negatively regulate PRC1 and LHX2, respectively [ 50 , 51 ]. LHX2 activates the Notch pathway and reduces radiosensitivity of NPC cells.…”

Section: Biological Functions Of Lncrna/circrna-mediated Cerna Networ...mentioning

confidence: 99%

Insight into LncRNA- and CircRNA-Mediated CeRNAs: Regulatory Network and Implications in Nasopharyngeal Carcinoma—A Narrative Literature Review

Zhang

Xin

et al. 2022

Cancers

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“…Axes were also identified involving newer, recently discovered lncRNAs and targets, such as PTPRG-AS1 (protein tyrosine phosphatase, receptor type, G (PTPRG) Antisense RNA 1). This lncRNA is involved in two axes: PTPRG-AS1/miR-124-3p/CCND1 in lung adenocarcinoma and PTPRG-AS1/miR-124-3/LHX2 in nasopharyngeal carcinoma, which promote cell proliferation, cell cycle in vitro/in vivo, moreover, activation of LHX2 (LIM Homeobox 2) induces Notch pathway and reduces radiosensitivity [ 56 , 89 ].…”

Section: Long Non-coding Rnas In Dysregulation Of Mir-124 Target Gene...mentioning

confidence: 99%

“…For 14 complete interactomes (HOTAIR/miR-124/ST8SIA4; HOXA11-AS/miR-124-3p/ITGB3; HOXA11-AS/miR-124/Sp1; KCNQ1OT1/miR-124-3p/TRIM14; LINC00240/miR-124-3p/DNMT3B; LINC00511/miR-124-3p/EZH2; LINC01410/miR-124-3p/SMAD5; MALAT1/miR-124/Capn4; MALAT1/miR-124/foxq1; SND1-IT1/miR-124/COL4A1; SNHG16/miR-124-3p/MCP-1; SP1- GCMA/miR-124/SLUG, SNAIL; UCA1/miR-124/JAG1; and XIST/miR-124/AR), involvement in EMT and/or development of metastasis in cancers of the corresponding localizations was revealed [ 43 , 59 , 62 , 63 , 64 , 65 , 67 , 70 , 73 , 76 , 90 , 91 , 93 , 94 ]. Moreover, the involvement of several interactomes (HOTTIP/miR-124-3p/HMGA2; NEAT1/miR-124/p65; MALAT1/miR-124/CDK4; MALAT1/miR-124/TGF-β1; MALAT1/miR-124/HBx; UCA1/miR-124/JAG1; PTPRG-AS1/miR-124-3/LHX2; OIP5-AS1/miR-124-5p/IDH2) into several signaling pathways, such as Wnt/b-catenin pathway, E2F1 signaling, TGF-β signaling, SMAD pathway, ERK/MAPK pathway, HIF-1α-pathway, Notch signaling, PI3K/Akt signaling, and cancer cell stemness has been established [ 60 , 74 , 78 , 80 , 82 , 87 , 89 , 93 ].…”

Section: Long Non-coding Rnas In Dysregulation Of Mir-124 Target Gene...mentioning

confidence: 99%

“…Besides, the KCNQ1OT1/miR-124-3p/TRIM14 and PDIA3P1/miR-124-3p/TRAF6 axes increase chemoresistance, PTPRG-AS1/miR-124-3/LHX2 reduces radiosensitivity, and LINC00240/miR-124-3p/STAT3 inhibits natural killer T (NKT) cell cytotoxicity, which is critical for successful anticancer therapy [ 64 , 66 , 88 , 89 ].…”

Section: Long Non-coding Rnas In Dysregulation Of Mir-124 Target Gene...mentioning

confidence: 99%

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Regulation of the Key Epithelial Cancer Suppressor miR-124 Function by Competing Endogenous RNAs

Брага

Фридман

Burdennyy

et al. 2022

IJMS

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A decrease in the miR-124 expression was observed in various epithelial cancers. Like a classical suppressor, miR-124 can inhibit the translation of multiple oncogenic proteins. Epigenetic mechanisms play a significant role in the regulation of miR-124 expression and involve hypermethylation of the MIR-124-1/-2/-3 genes and the effects of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) according to the model of competing endogenous RNAs (ceRNAs). More than 40 interactomes (lncRNA/miR-124/mRNA) based on competition between lncRNAs and mRNAs for miR-124 binding have been identified in various epithelial cancers. LncRNAs MALAT1, NEAT1, HOXA11-AS, and XIST are the most represented in these axes. Fourteen axes (e.g., SND1-IT1/miR-124/COL4A1) are involved in EMT and/or metastasis. Moreover, eight axes (e.g., OIP5-AS1/miR-124-5p/IDH2) are involved in key pathways, such as Wnt/b-catenin, E2F1, TGF-β, SMAD, ERK/MAPK, HIF-1α, Notch, PI3K/Akt signaling, and cancer cell stemness. Additionally, 15 axes impaired patient survival and three axes reduced chemo- or radiosensitivity. To date, 14 cases of miR-124 regulation by circRNAs have been identified. Half of them involve circHIPK3, which belongs to the exonic ecircRNAs and stimulates cell proliferation, EMT, autophagy, angiogenesis, and multidrug resistance. Thus, miR-124 and its interacting partners may be considered promising targets for cancer therapy.

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Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

Zhang,

Wang,

et al. 2023

J Biochem & Molecular Tox

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Esophageal cancer (EC) is a challenging tumor to treat with radiotherapy, often exhibiting resistance to this treatment modality. To explore the factors influencing radioresistance, we focused on the role of hypoxia‐induced factor‐1α (HIF‐1α), and its interaction with the long noncoding RNA long intergenic nonprotein coding RNA 1116 (LINC01116). We analyzed the LINC01116 expression in EC and EC cell lines/human normal esophageal epithelial cell line (Het‐1A). LINC01116 was silenced/overexpressed in EC109/KYSE30 cells under hypoxia, followed by radioresistance assessment. We measured HIF‐1α levels in hypoxic EC cells and further validated the binding of HIF‐1α with LINC01116, analyzing their interaction in EC cells. We then performed experiments in EC109 cells by transfection them with sh‐HIF‐1α/oe‐LINC01116 to verify the effects. Additonally, we analyzed the localization of LINC01116 and its binding with miR‐3612, followed by a combined experiment performed to validate the results. Our findings indicated that LINC01116 was highly expressed in EC and further elevated in hypoxic EC cells. LINC01116 was expressed at a high level in EC, which was further elevated in EC cells under hypoxic conditions. Knockdown of LINC01116 triggered EC cell apoptosis, thus suppressing radioresistance. Further investigation revealed that HIF‐1α transcriptionally activated LINC01116 expression under hypoxia, and silencing HIF‐1α lowered EC cell radioresistance by downregulating LINC01116. Under hypoxic conditions, LINC01116 could function as a sponge for miR‐3612 and inhibit its expression. This interaction between LINC01116 and miR‐3612 played a crucial role in mediating radioresistance in EC cells. Briefly, under hypoxic conditions, HIF‐1α facilitates radioresistance of EC cells by transcriptionally activating LINC01116 expression and downregulating miR‐3612.

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Long non-coding RNA PTPRG-AS1/microRNA-124-3p regulates radiosensitivity of nasopharyngeal carcinoma via the LIM Homeobox 2-dependent Notch pathway through competitive endogenous RNA mechanism

Cited by 10 publications

References 38 publications

Insight into LncRNA- and CircRNA-Mediated CeRNAs: Regulatory Network and Implications in Nasopharyngeal Carcinoma—A Narrative Literature Review

Insight into LncRNA- and CircRNA-Mediated CeRNAs: Regulatory Network and Implications in Nasopharyngeal Carcinoma—A Narrative Literature Review

Regulation of the Key Epithelial Cancer Suppressor miR-124 Function by Competing Endogenous RNAs

Hypoxia‐induced factor‐1α promotes radioresistance of esophageal cancer cells by transcriptionally activating LINC01116 and suppressing miR‐3612 under hypoxia

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