Cancer progression including proliferation, metastasis, and chemoresistance has become a serious hindrance to cancer therapy. This phenomenon mainly derives from the innate insensitive or acquired resistance of cancer cells to apoptosis. Ferroptosis is a newly discovered mechanism of programmed cell death characterized by peroxidation of the lipid membrane induced by reactive oxygen species. Ferroptosis has been confirmed to eliminate cancer cells in an apoptosis-independent manner, however, the specific regulatory mechanism of ferroptosis is still unknown. The use of ferroptosis for overcoming cancer progression is limited. Noncoding RNAs have been found to play an important roles in cancer. They regulate gene expression to affect biological processes of cancer cells such as proliferation, cell cycle, and cell death. Thus far, the functions of ncRNAs in ferroptosis of cancer cells have been examined, and the specific mechanisms by which noncoding RNAs regulate ferroptosis have been partially discovered. However, there is no summary of ferroptosis associated noncoding RNAs and their functions in different cancer types. In this review, we discuss the roles of ferroptosis-associated noncoding RNAs in detail. Moreover, future work regarding the interaction between noncoding RNAs and ferroptosis is proposed, the possible obstacles are predicted and associated solutions are put forward. This review will deepen our understanding of the relationship between noncoding RNAs and ferroptosis, and provide new insights in targeting noncoding RNAs in ferroptosis associated therapeutic strategies.

Objective. Invasive breast cancer can be metastasized through axillary lymph nodes (LNs). This study was to evaluate the effectiveness of quantitative shear wave elastography (SWE) to predict axillary LN metastasis, which also provides prognostic implication of SWE as a histopathologic element of invasive breast cancer. Methods. 72 prospectively enrolled patients received B-mode ultrasound (BUS) and SWE, and the elasticity index (EI) of SWE at the stiffest part of lymph nodes (LNs) was measured. EI of SWE was closely associated with pathologic results and the histopathologic elements. The receiver operating characteristics (ROC) curve was drawn to evaluate the optimal cut-off value for the assessment of disease severity. Results. A significantly longer short-axis diameter and a larger maximal cortex were observed in malignant LNs than that in healthy LNs. The absence of the hilum was associated with metastatic LNs. The EI of SWE varied markedly between the benign and malignant LNs. The combination of E_{max and} BUS showed higher area under the curve (AUC) than BUS alone to predict metastatic LNs (0.7762 vs. 0.7230). EI of SWE in malignant lymph nodes those with extranodal extension are higher than those without extranodal extension. Conclusions. Quantitative SWE provides a viable alternative for the assessment of axillary LN and shows great potential to predict pathological prognostic elements of metastatic axillary LNs in invasive breast cancer. Joint use of SWE and BUS allows examination of the predictive outcome of BUS for axillary lymph node metastasis in invasive breast cancer.

Hepatocellular carcinoma (HCC) recurrence following microwave ablation poses a pressing clinical challenge, driven by metabolically adapted residual cells that establish an immunosuppressive tumour microenvironment. Our study identifies the post-ablation upregulation of fumarylacetoacetate hydrolase (FAH) as a crucial "metabolic checkpoint" promoting relapse. Elevated FAH expression results in increased fumarate levels within residual HCC cells, supporting tumour cell survival by enhancing energy metabolism while concurrently impairing CD8⁺ T cell function. Mechanistically, fumarate binds to and stabilises heat shock protein 70 (HSP70), establishing a thermal ablation induced FAH-fumarate-HSP70 axis that drives immunosuppression. To counteract this pivotal axis, we engineered a gallium-based functionalized nanoplatform. This system incorporates a lactate oxidase shell that responds to the lactate-rich tumour microenvironment, enabling the site-specific co-release of Ga³⁺, FAH-silencing plasmids and the glycolysis inhibitor 2-deoxy-D-glucose. Our nanoplatforms disrupt the FAH-fumarate-HSP70 axis to eradicate residual HCC, activate CD8⁺ T cells, and restore immunity, targeting recurrence dysregulation while integrating metabolic blockade with immunomodulation to prevent post-ablation relapse with clinical translation potential.

Hepatocellular carcinoma (HCC) recurrence following microwave ablation poses a pressing clinical challenge, driven by metabolically adapted residual cells that establish an immunosuppressive tumour microenvironment. Our study identifies the post-ablation upregulation of fumarylacetoacetate hydrolase (FAH) as a crucial metabolic checkpoint promoting relapse. Elevated FAH expression results in increased intra- and extracellular fumarate levels within residual HCC cells, supporting tumour cell survival by enhancing Krebs cycle activity while concurrently impairing CD8⁺ T cell function. Mechanistically, fumarate binds to and stabilises heat shock protein 70 (HSP70), establishing an ablation-induced FAH–fumarate–HSP70 axis that drives immunosuppression. To counteract this pivotal axis, we engineered a novel gallium-based functionalized nanoplatform. This system incorporates a lactate oxidase shell that responds to the lactate-rich tumour microenvironment, enabling the site-specific co-release of FAH-silencing plasmids and the glycolysis inhibitor 2-deoxy-D-glucose. Our stratified nanoplatforms, designed to disrupt the FAH–fumarate–HSP70 axis, achieve synergistic eradication of residual HCC cells, promote CD8⁺ T cell activation, and restore anti-tumour immunity through coordinated metabolic intervention. This unique design specifically targets the metabolic and immune dysregulation underlying HCC recurrence, integrating metabolic blockade with immunomodulation to offer a highly effective strategy for preventing post-ablation relapse and holds significant potential for clinical translation.