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Osteosarcoma (OS) represents a highly aggressive malignant neoplasm of the bone, predominantly affecting pediatric and adolescent populations. Despite significant advancements in surgical techniques and chemotherapeutic regimens, patient prognoses remain suboptimal, primarily due to elevated rates of metastasis and the development of chemoresistance. Circular RNAs (circRNAs), a class of stable and tissue-specific non-coding RNAs, have emerged as critical regulators in diverse biological processes, including autophagy—a crucial mechanism implicated in tumor progression and therapeutic resistance. This review systematically summarizes the multifaceted roles of circRNAs in the initiation and progression of osteosarcoma, with a central focus on the molecular mechanisms by which circRNAs modulate cellular proliferation, migration, invasion, metastasis, and above all, chemotherapy resistance. Special attention is given to the interaction between circRNAs and autophagy pathways (e.g., PINK1/Parkin and PI3K/AKT signaling), underscoring the dual roles of circRNAs in both facilitating tumor survival via modulating cytoprotective autophagy and inducing autophagic cell death in OS. Furthermore, the potential of circRNAs as non-invasive diagnostic biomarkers, prognostic indicators, and therapeutic targets is examined, with an emphasis on their capacity to modulate miRNA sponging and downstream signaling pathways. Despite these promising advancements, several key challenges remain in the clinical translation of circRNA-targeted strategies for OS management.

Intervertebral disc degeneration (IDD) is a chronic progressive condition mainly caused by excessive inflammatory cytokines. Berberine (BBR) exerts anti-inflammatory effect on diseases and protective effect against IDD. However, the mechanism is not uncertain. This study is aimed at investigating the molecular mechanism of BBR on IDD. Nucleus pulposus (NP) cells were treated with BBR at different concentrations. The IDD rat model was established by acupuncture. The effect of BBR on interleukin- (IL-) 1β-induced cell proliferation was measured by CCK-8 assay and BrdU staining. The role of BBR in IL-1β-induced apoptosis, autophagy repression, and extracellular matrix (ECM) degradation was measured by Annexin/PI staining, immunofluorescence, and immunoblot. The effect of BBR on IDD was investigated in rat. Our findings showed that BBR restored cell growth and attenuated apoptosis in IL-1β-induced NP cells. BBR also prevented the IL-1β-induced ECM degradation through regulating ECM-related enzymes and factors. Additionally, BBR significantly activated autophagy repressed by IL-1β. Autophagy stimulated by BBR was diminished by the inhibition of the AMPK/mTOR/Ulk1 signaling pathway. In vivo study also showed BBR attenuated intervertebral disc degeneration. BBR could attenuate NP cells apoptosis and ECM degradation induced by IL-1β through autophagy by the AMPK/mTOR/Ulk1 pathway. This study suggests BBR might function as an AMPK activator to alleviate IDD progression.