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Elucidating the Pro-Tumor Role of LncRNA CROCCP2 in Glioma via the miR-5584-5p/HOXD11/Autophagy Pathway
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DOI：10.1111/cas.70433.png)
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Abstract
En 中文
Glioma is the most common primary malignant tumor of the central nervous system, characterized by high invasiveness and a high recurrence rate. The clinical therapeutic efficacy remains limited, necessitating the exploration of novel molecular mechanisms and therapeutic targets. Long non-coding RNAs (lncRNAs), as key epigenetic regulators in tumor progression, can influence tumorigenesis and development through lncRNA–miRNA–mRNA regulatory axes. Here, we reveal the critical role of the lncRNA CROCCP2/miR-5584-5p/HOXD11 axis in glioma. LncRNA CROCCP2 was significantly upregulated in glioma tissues and cell lines, in vitro, markedly promoting the proliferation, migration, and invasion of glioma cells. Mechanistically, LncRNACROCCP2 acts as a competing endogenous RNA to sponge miR-5584-5p, thereby relieving its suppression of the target gene HOXD11, leading to HOXD11 upregulation. HOXD11 negatively regulated autophagy, as reflected by reduced LC3B-II and Beclin1 levels and increased p62 expression. Conversely, CROCCP2 or HOXD11 knockdown activated autophagy and provided supportive evidence for ongoing autophagic flux based on the addition of LC3B-II and p62 after bafilomycin A1 treatment. Knockdown of either lncRNA CROCCP2 or HOXD11 suppressed glioma cell proliferation, migration, and invasion in vitro. In addition, HOXD11 silencing markedly inhibited subcutaneous and intracranial tumor growth in nude mice; furthermore, HOXD11 knockout can even halt the growth of subcutaneous tumors. Collectively, our findings suggest that the lncRNA CROCCP2/miR-5584-5p/HOXD11 axis contributes to glioma cell malignant phenotypes in vitro and tumor growth in vivo, at least partly through negative regulation of autophagy, providing a potential molecular target for glioma therapy.
Keywords:
autophagy
glioma
HOXD11
LncRNA CROCCP2
miR-5584-5p
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