RETRACTED: MiR-365a-3p-Mediated Regulation of HELLS/GLUT1 Axis Suppresses Aerobic Glycolysis and Gastric Cancer Growth

Yang, Rui; Liu, Gen; Han, Limin; Qiu, Yuheng; Wang, Lulin; Wang, Mei

doi:10.3389/fonc.2021.616390

Cited by 14 publications

(10 citation statements)

References 39 publications

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“…addition, high levels of LSH correlates with a poor prognosis in gastric cancer [72]. The mechanism associated with this observation might act through reduced levels of miR-365a-3p, since this microRNA binds to its 3' untranslated region (UTR) of the HELLS transcript and represses its translation, thereby resulting in reduced LSH levels and enhanced carcinogenesis [73].…”

Section: Lsh Is a Bridge Regulator In Oncogenesismentioning

confidence: 99%

Lymphoid-specific helicase in epigenetics, DNA repair and cancer

Chen

Rubio

et al. 2021

Br J Cancer

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Lymphoid-specific helicase (LSH) is a member of the SNF2 helicase family of chromatin-remodelling proteins. Dysfunctions or mutations in LSH causes an autosomal recessive disease known as immunodeficiency-centromeric instability-facial anomaly (ICF) syndrome. Interestingly, LSH participates in various aspects of epigenetic regulation, including nucleosome remodelling, DNA methylation, histone modifications and heterochromatin formation. Further, LSH plays a crucial role during DNA-damage repair, specifically during double-strand break (DSB) repair, since murine LSH was shown to be essential for non-homologous end joining (NHEJ) and homologous recombination (HR). Accordingly, overexpression of LSH drives tumorigenesis and malignancy. On the other hand, LSH homologs stabilise the genome. Thus, LSH might be implemented as a biomarker for various cancer types and potential target molecule to develop therapeutic strategies against them. In this review, we focus on the role of LSH in orchestrating chromatin rearrangements, such as DNA methylation and histone modifications, as well as in DNA-damage repair. Changes in chromatin structure may facilitate gene expression signatures that cause malignant transformation. We summarise recent findings of LSH in cancers and raise critical open questions for further studies.

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Section: Lsh Is a Bridge Regulator In Oncogenesismentioning

confidence: 99%

Lymphoid-specific helicase in epigenetics, DNA repair and cancer

Chen

Rubio

et al. 2021

Br J Cancer

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“…Previous bioinformatic studies have identified amounts of GC related miRNAs (3,(5)(6)(7)(8). Some circulating serum exosomal miRNAs were proposed as novel biomarkers for GC diagnosis, such as miR-92a-3p, miR-500a-3p, miR-1246, and miR-423-5p (3,5,(9)(10)(11)(12).…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Circulating Exosomal microRNAs in Gastric Cancer

et al. 2021

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Exosomal miRNAs (EmiRs) can be used for prediction of gastric cancer (GC) development. Supposedly, both plasma and urinary microRNAs can also be potential biomarkers for screening, but the diagnostic values of EmiRs in blood and urine are not fully studied. We here collected both types of samples from GC patients and healthy individuals and conducted miRNA sequencing to identify key members of EmiRs in GC. The exosomes samples derived from blood and urine were collected from 3 healthy individuals and 7 GC patients. Differentially expressed miRNAs (DEmiRNAs) were acquired, ontology enrichment analysis and Protein-protein Interaction (PPI) enrichment analysis were performed. There were 8 DEmiRNAs in the serum and 3 DEmiRNAs in the urine. For GC patients, there were three up-regulated DEmiRNAs (hsa-miR-130b-3p, hsa-miR-151a-3p and hsa-miR-15b-3p) in the serum exosomes, and one up-regulated DEmiRNA (hsa-miR-1246) in the urinary exosomes. Using miRNA target prediction databases, we found 418 common targets of hsa-miR-15b-3p, 35 common targets of hsa-miR-151a-3p, 117 common targets of hsa-miR-130b-3p, and 357 common targets of hsa-miR-1246. Some commonly enriched ontology terms were found, including GO BP terms like cell surface receptor signaling pathway involved in cell-cell signaling, positive regulation of catabolic process, morphogenesis of an epithelium, and GO CC terms perinuclear region of cytoplasm. The PPI network show some key nodes, including TAOK1, CMTM6, SCN3A, WASF3, IGF1, CNOT7, GABRG1, PRKD1. Together, this study provided an integrative analysis of expression profile of key circulating exosomal microRNAs. Four key exosomal miRNAs (hsa-miR-130b-3p, hsa-miR-151a-3p and hsa-miR-15b-3p) and the interaction network or enrichments based on their targets (TAOK1, CMTM6, SCN3A, WASF3, IGF1, CNOT7, GABRG1, PRKD1) may provide a reference of the molecular mechanisms in the GC development.

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“…It was reported that miR-365a-3p acts as a cancer suppressor gene in various cancers [22,38,39]. Therefore, we investigated whether miR-365a-3p inhibits OS growth.…”

Section: Mir-365a-3p Targeted Pgk1 Directly In Os Cells and Inhibited Os Growthmentioning

confidence: 99%

LncRNA HCG18 promotes osteosarcoma growth by enhanced aerobic glycolysis via the miR-365a-3p/PGK1 axis

Pan

Guo²,

Liu

et al. 2022

Cell Mol Biol Lett

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Background Osteosarcoma (OS) is a common primary bone malignancy. Long noncoding RNA HCG18 is known to play an important role in a variety of cancers. However, its role in OS and relevant molecular mechanisms are unclear. Methods Real-time quantitative PCR was performed to determine the expression of target genes. Function experiments showed the effects of HCG18 and miR-365a-3p on OS cell growth. Results HCG18 expression was increased in OS cell lines. Moreover, in vitro and in vivo experiments demonstrated that HCG18 knockdown inhibited OS cell proliferation. Mechanistically, HCG18 was defined as a competing endogenous RNA by sponging miR-365a-3p, thus elevating phosphoglycerate kinase 1 (PGK1) expression by directly targeting its 3ʹUTR to increase aerobic glycolysis. Conclusion HCG18 promoted OS cell proliferation via enhancing aerobic glycolysis by regulating the miR-365a-3p/PGK1 axis. Therefore, HCG18 may be a potential target for OS treatment.

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RETRACTED: MiR-365a-3p-Mediated Regulation of HELLS/GLUT1 Axis Suppresses Aerobic Glycolysis and Gastric Cancer Growth

Cited by 14 publications

References 39 publications

Lymphoid-specific helicase in epigenetics, DNA repair and cancer

Lymphoid-specific helicase in epigenetics, DNA repair and cancer

Identification of Key Circulating Exosomal microRNAs in Gastric Cancer

LncRNA HCG18 promotes osteosarcoma growth by enhanced aerobic glycolysis via the miR-365a-3p/PGK1 axis

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