SET domain-containing 5 is a potential prognostic biomarker that promotes esophageal squamous cell carcinoma stemness

Piao, Lihua; Li, Haoyue; Feng, Ying; Yang, Zheng; Kim, Seokhyung; Xuan, Yanhua

doi:10.1016/j.yexcr.2020.111861

Cited by 16 publications

(17 citation statements)

References 41 publications

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“…The involvement of SETD5 in the MEK-ERK pathway was also observed in non-small cell lung cancer ( Yu et al, 2019 ). In addition, SETD5 promoted cancer stem cell properties and PI3K-Akt-mTOR axis activity in esophageal squamous cell carcinoma (ESCC) ( Piao et al, 2020 ) and breast cancer ( Yang et al, 2021 ). More interestingly, SETD5 expression in ESCC was positively correlated with HIF-1α levels, which regulate glycolytic activity ( Piao et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Molecular analyses proposed that SETD5 might function through its interaction with the HDAC3 and PAF1 complexes ( Deliu et al, 2018 ; Osipovich et al, 2016 ). More recently, SETD5 was shown to be involved in different cancers ( Piao et al, 2020 ; Sowalsky et al, 2015 ; Yu et al, 2019 ; Yang et al, 2021 ). These studies demonstrate that SETD5 is implicated in aggressive tumorigenic progression.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells

Park

Moon

Kim

et al. 2022

Molecules and Cells

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Hepatocellular carcinoma (HCC) is an aggressive and incurable cancer. Although understanding of the molecular pathogenesis of HCC has greatly advanced, therapeutic options for the disease remain limited. In this study, we demonstrated that SETD5 expression is positively associated with poor prognosis of HCC and that SETD5 depletion decreased HCC cell proliferation and invasion while inducing cell death. Transcriptome analysis revealed that SETD5 loss downregulated the interferon-mediated inflammatory response in HCC cells. In addition, SETD5 depletion downregulated the expression of a critical glycolysis gene, PKM (pyruvate kinase M1/2), and decreased glycolysis activity in HCC cells. Finally, SETD5 knockdown inhibited tumor growth in xenograft mouse models. These results collectively suggest that SETD5 is involved in the tumorigenic features of HCC cells and that targeting SETD5 may suppress HCC progression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells

Park

Moon

Kim

et al. 2022

Molecules and Cells

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“… 50 It is also a potential prognostic biomarker that promotes esophageal squamous cell carcinoma stemness. 51 Whole transcriptome sequencing has shown that increased SETD5 expression levels are present in metastatic castration-resistant prostate cancer. 33 SETD5-coordinated chromatin reprogramming regulates adaptive resistance to targeted pancreatic cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

CircRNA PTPRM Promotes Non-Small Cell Lung Cancer Progression by Modulating the miR-139-5p/SETD5 Axis

Jiang

Zhao

Zou

et al. 2022

Technol Cancer Res Treat

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Introduction: Circular RNAs (circRNAs) are important regulators in various cancers, especially hepatocellular carcinoma. However, the role of circ RNA PTPRM (circPTPRM) in the development of non-small-cell lung cancer (NSCLC) remains unclear. Methods: We collected 26 clinical specimens (corresponding to 26 normal lung tissues) of lung adenocarcinoma and the expression of mir-139-5p and circPTPRM were first detected. Cell proliferation was detected by EdU method, invasion/migration ability of cells was evaluated by transwell method. And the correlation between circPTPRM and mir-139-5p was detected by luciferase reporter gene and RNA pull-down assay. Finally, we verified our hypothesis with BALB/c nude mice. Results: Through bioinformatics software, we found that circPTPRM was negatively correlated with mir-139-5p, and then we used human adenocarcinoma tissue samples to further verify their relationship and get the same result. EdU method, transwell method, and luciferase assay, RNA pull-down assay were applied, and the results show that the knockdown of circPTPRM inhibit proliferation, migration, and invasion of cells can be reversed by mir-139-5p inhibitor. Next, we used Starbase v2.0 to identify the target site of miR-139-5p and focused on SET domain containing 5 (SETD5). We derive the hypothesis by verifying the relationship between miR-139-5p and SETD5 that circPTPRM may interact with miR-139-5p/SETD5 axis. At last, we evaluated the effects of circPTPRM, SETD5, and miR-139-5p on tumor growth in vivo using BALB/c nude mice to prove the hypothesis. Conclusion: We thus conclude that circPTPRM promotes the progression of NSCLC by regulating the miR-139-5p/SETD5 axis.

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“…SRGAP3 enables GTPase activator activity and participates in negative regulation of cell migration [ 35 ]. SETD5 may function as a histone methyltransferase and promote cell stemness of esophageal squamous cell carcinoma and NSCLC [ 36 , 37 ]. OXTR belongs to the G-protein coupled receptor family and acts as a receptor for oxytocin.…”

Section: Discussionmentioning

confidence: 99%

Linc00312 Single Nucleotide Polymorphism as Biomarker for Chemoradiotherapy Induced Hematotoxicity in Nasopharyngeal Carcinoma Patients

Guo

Wang

et al. 2022

Disease Markers

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Background. Linc00312 is downregulated in nasopharyngeal carcinoma (NPC) and associates with poor treatment efficacy. Genetic variations are the main cause of individual differences in treatment response. The objective of this study is to explore the relationship between genetic variations of linc00312 and the risk of chemoradiotherapy induced toxic reactions in NPC patients. Methods. We used a bioinformatics approach to select 3 single nucleotide polymorphisms (SNPs) with regulatory feature in linc00312 (rs12497104, rs15734, and rs164966). 505 NPC patients receiving chemoradiotherapy with complete follow-up data were recruited. Genotyping was carried out by MassARRAY iPLEX platform. Univariate logistic and multivariate logistic regression were used to analyze the risk factors responsible for toxic reactions of NPC patients. Results. Our result demonstrated that linc00312 rs15734 ( G > A ) was significantly associated with severe leukopenia in NPC patients underwent chemoradiotherapy (AA vs. GG, OR = 3.145 , P = 0.029 ). In addition, the risk of severe leukopenia was remarkably increased to 5.635 times ( P = 0.034 ) in female with rs15734 AA genotype compared to male with rs15734 GG genotype. Moreover, patients with rs12497104 ( G > A ) AA genotype showed a 67.5% lower risk of thrombocytopenia than those with GG genotype ( P = 0.030 ). Remarkably, the younger patients ( age < 47 ) with rs12497104 AA genotype displayed a 90% decreased risk of thrombocytopenia compared with older patients ( age ≥ 47 ) carrying rs12497104 GG genotype ( P = 0.030 ). Conclusions. Genetic variations of linc00312 affect the risk of chemoradiotherapy induced hematotoxicity in nasopharyngeal carcinoma patients and may serve as biomarkers for personalized medicine.

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SET domain-containing 5 is a potential prognostic biomarker that promotes esophageal squamous cell carcinoma stemness

Cited by 16 publications

References 41 publications

Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells

Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells

CircRNA PTPRM Promotes Non-Small Cell Lung Cancer Progression by Modulating the miR-139-5p/SETD5 Axis

Linc00312 Single Nucleotide Polymorphism as Biomarker for Chemoradiotherapy Induced Hematotoxicity in Nasopharyngeal Carcinoma Patients

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