Deciphering the oncogenic network: how C1QTNF1-AS1 modulates osteosarcoma through miR-34a-5p and glycolytic pathways

Deciphering the oncogenic network: how C1QTNF1-AS1 modulates osteosarcoma through miR-34a-5p and glycolytic pathways

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IntroductionOsteosarcoma (OS), a prevalent metastatic cancer among young individuals, is associated with a grim prognosis.Long non-coding RNAs (lncRNAs), including C1QTNF1-AS1, are pivotal regulators of cancer cell proliferation and motility.As an oncogene, C1QTNF1-AS1 is implicated in various tumor types, such as colorectal, pancreatic, hepatocellular carcinomas, and OS.The aim of this study was to investigate the functions and underlying mechanisms of C1QTNF1-AS1 in the progression of osteosarcoma.

MethodsThis investigation focused on elucidating the functional roles and mechanisms of C1QTNF1-AS1 in OS cells.Bioinformatics tools were utilized to identify the interaction between microRNA miR-34a-5p and C1QTNF1-AS1, as well as the targeting of LDHA and PDK3 by miR-34a-5p.Dual-luciferase reporter assays and RNA immunoprecipitation were employed to validate these interactions.Expression profiles of C1QTNF1-AS1, miR-34a-5p, LDHA, and PDK3 in osteosarcoma cells were analyzed using RT-PCR and western blot analyses, revealing their intricate relationships.

The impact of these molecules on OS cell proliferation, invasion, Arm Guards and migration was assessed through CCK-8, Transwell, and Cell scratch assay.Moreover, the effects on aerobic glycolysis in OS cells were examined by quantifying ATP levels, lactate production, glucose uptake capacity, and the extracellular acidification rate.ResultsThe findings indicated a significant decrease in C1QTNF1-AS1 expression levels in OS cells compared to normal osteoblasts.A parallel downregulation trend of miR-34a-5p was also observed in OS cells.

Silencing C1QTNF1-AS1 led to a marked upregulation of LDHA and PDK3 in OS cells, which was partially attenuated by miR-34a-5p mimics.Functional evaluations demonstrated that suppression Hat Bands of C1QTNF1-AS1 accelerated OS cell growth, motility, invasiveness, and the Warburg effect.Conversely, the overexpression of miR-34a-5p mitigated these stimulatory effects, suggesting a regulatory role in modulating OS progression.DiscussionOur research emphasizes the critical role of C1QTNF1-AS1 in the pathogenesis of osteosarcoma (OS).

We discovered that the downregulation of C1QTNF1-AS1 indirectly upregulates the expression of LDHA and PDK3 by suppressing miR-34a-5p, which functions as a regulator of the Warburg effect.This cascade of events promotes OS progression by enhancing glycolytic metabolism and supplying energy for cancer cell growth, migration, and invasion.These findings suggest a potential therapeutic target and highlight the importance of understanding the regulatory network involving lncRNAs in cancer metabolism and progression.