Oncolytic viruses (OVs) represent a promising immunotherapy for cancer treatment, though their clinical application is often limited by systemic toxicity and low immunogenicity. To address this, we developed NDV-GT, a genetically engineered Newcastle disease virus that encodes porcine α-1,3-galactosyltransferase. These epitopes are recognized by pre-existing natural antibodies, triggering a hyperacute rejection response characterized by complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC). Furthermore, NDV-GT modulates the tumor microenvironment by promoting T-cell infiltration and cytokine secretion, converting immunologically "cold" tumors into "hot" ones. Mechanistically, the virus inhibits PI3K/AKT and NF-κB signaling pathways, inducing apoptosis and suppressing tumor proliferation. In a preliminary clinical study of 20 patients with advanced refractory carcinomas, NDV-GT achieved a 90.0% disease control rate with no serious adverse events, underscoring its potential as a novel, safe, and effective oncolytic agent that elicits robust antitumor immunity.

High-dose ionizing radiation (IR), as encountered in radiotherapy-related and radiological emergency contexts, induces severe acute developmental and neurobehavioral toxicity. However, safe and effective natural radioprotective agents remain limited. Ferulic acid (FA), a natural phenolic compound widely found in medicinal and edible plants, possesses well-established antioxidant and anti-inflammatory properties. Nevertheless, its protective effects and underlying mechanisms against high-dose IR-induced acute in vivo injury remain largely unclear. This study aimed to evaluate the in vivo protective effects of FA against acute IR-induced developmental and neurobehavioral toxicity in zebrafish and to investigate the involvement of apoptosis-related pathways. An acute radiation injury model was established in zebrafish embryos subjected to 1-10 Gy IR treatment, and 2.5 Gy was selected for FA intervention based on the dose-response results. Developmental phenotyping, locomotor activity, and social behavioral assays were conducted to assess IR-induced toxicity. Transcriptomic profiling combined with GO and KEGG enrichment analyses, RT-qPCR validation, and acridine orange staining were performed to explore the potential molecular mechanisms. High-dose IR treatment induced dose-dependent developmental defects, increased mortality, and pronounced locomotor and social behavioral abnormalities in zebrafish larvae. FA treatment significantly alleviated IR-induced developmental toxicity and improved locomotor activity and light-dark transition responses. Transcriptomic analysis showed that FA was associated with broad modulation of IR-responsive gene expression changes, with apoptosis, organelle homeostasis, and cell cycle-related processes identified as major transcriptomic features. Four apoptosis-associated candidate genes (chchd10, dmtf1, rcn3, and nr3c2) were identified and validated under irradiated conditions. FA attenuated the aberrant expression of these genes and reduced excessive apoptosis-associated signals in vivo. Collectively, these findings demonstrate that FA confers significant protection against high-dose IR-induced acute in vivo toxicity, at least in part, in association with apoptosis-related transcriptional modulation and attenuation of apoptosis-associated signals. This study provides mechanistic insights supporting FA as a promising natural radioprotective agent for further evaluation in radiotherapy-related and radiological emergency contexts.

Cervical squamous cell carcinoma (CESC) is one of the most common cancers in women, and radiotherapy has been used as a primary treatment. However, its efficacy is limited by intrinsic and acquired radiation resistance. Our previous study demonstrated that Deoxycytidine kinase (dCK) inhibits ionizing radiation (IR)-induced cell death, including apoptosis and mitotic catastrophe, and dCK is a HSP90-interacting protein by mass spectrometry and co-immunoprecipitation assay. In the present study, we found that dCK inhibited IR-induced ferroptosis by increasing the activity and stability of SLC7A11. Using the E3 ubiquitin ligase database (UbiBrowser), we predicted NEDD4L as a potential ubiquitin ligase of dCK, and WWP1/2 as potential ubiquitin ligases of NEDD4L, respectively. These predictions were subsequently verified through a ubiquitination IP assay. Our findings indicate that HSP90 regulates dCK stability by inhibiting NEDD4L through the recruitment of ubiquitin ligases WWP1/2. In summary, our study reveals the HSP90-WWP1/WWP2-NEDD4L-dCK-SLC7A11 axis as a critical regulator of IR-induced ferroptosis in HeLa cells. These findings provide valuable insights into potential strategies for the radiosensitization of cervical cancer.

Background: Intervertebral disc degeneration (IDD) is a major cause of low back pain, with cartilaginous endplate (CEP) degeneration playing a critical role. While Yes-associated protein (YAP) and its involvement in CEP degeneration and ferroptosis remain unclear. This study aimed to investigate the regulatory role of YAP in CEP ferroptosis and its underlying mechanisms. Methods: YAP expression was analyzed in human CEP tissues and mouse LSI models. CEP cells were treated with Verteporfin or YAP-siRNA. Ferroptosis was assessed by measuring iron levels, lipid peroxidation, GSH content, and viability assays. Molecular mechanisms were elucidated using CUT&RUN-qPCR, dual-LUC, and immunofluorescence colocalization. Verteporfin (VP) therapeutic efficacy was evaluated in LSI mice. Results: YAP knockdown attenuated oxidative stress-induced CEP chondrocyte degeneration and ferroptosis features. Mechanistically, we identified that oxidative stress-induced CEP chondrocyte degeneration involves ferritinophagy, which is regulated by the YAP/TEAD1 signaling axis through transcriptional control of nuclear coactivator 4 (NCOA4). Treatment with verteporfin, a YAP/TEAD1 axis inhibitor, effectively reduced CEP chondrocyte degeneration and IDD progression by targeting NCOA4-mediated ferritinophagy. Conclusion: Through detailed molecular and cellular analyses, we revealed that the YAP/TEAD1/NCOA4 signaling axis plays a crucial role in regulating CEP chondrocyte ferroptosis and IDD development. These findings not only enhance our understanding of IDD pathogenesis but also suggest that targeting the YAP/TEAD1/NCOA4 axis could be a promising therapeutic strategy for treating IDD. The Translational Potential of this Article: This study reveals YAP as a novel therapeutic target for intervertebral disc degeneration by regulating ferroptosis in cartilage endplate cells, which provides a novel strategy in the prevention of IDD.

This investigation delineates the differential impact of recurrence patterns—specifically, anastomotic recurrence (AR) and lymph node recurrence (LNR)—on the survival outcomes of patients with esophageal squamous cell carcinoma (ESCC). Additionally, it assesses the therapeutic efficacy of adjuvant radiotherapy in modifying these postoperative recurrence dynamics to inform optimized clinical management. A retrospective cohort analysis was conducted on 434 patients who developed recurrent ESCC following radical surgery at Shandong Cancer Hospital, from July 2018 through December 2022. Comprehensive clinical data were analyzed using logistic and Cox proportional hazards regression models to elucidate the risk factors associated with AR and LNR. Of the patients analyzed, 118 exhibited AR post-surgery. Multivariate logistic regression identified advanced N stage and the presence of LNR as predominant risk factors influencing recurrence. Survival analysis, employing Kaplan–Meier estimates, demonstrated a median survival time (MST) of 21 months (range: 1.6–146.1 months) for patients with AR. In patients experiencing LNR, Cox regression analyses revealed tumor location and the application of adjuvant radiotherapy as critical determinants of survival outcomes. Significantly, adjuvant radiotherapy markedly reduced the incidence of LNR, thereby attenuating overall recurrence rates. Postoperative recurrence significantly compromises survival in ESCC, underscoring the critical need for precise risk stratification and proactive management. This study substantiates the prognostic significance of adjuvant radiotherapy in reducing recurrence, providing pivotal insights for tailoring treatment protocols to enhance patient prognoses in ESCC.

Hepatocellular carcinoma is one of the most common malignant tumors, and radiotherapy plays a pivotal role in its therapeutic regimen. However, radiotherapy resistance is the main cause of therapeutic failure in patients. Our previous study revealed that Adiponectin Receptor 1 (AdipoR1) is involved in regulating radiation resistance in liver cancer patients treated with stereotactic body radiotherapy. To explore the mechanism, we performed high-throughput transcriptome sequencing of hepatocellular carcinoma cells with stable knockdown of AdipoR1. KEGG enrichment analysis indicated that the cell cycle and ubiquitination degradation pathways may be involved in the regulation of radiation resistance by AdipoR1.The knockdown of AdipoR1 can attenuate the radiation-induced G2/M phase arrest through cyclin B1.By the ubiquitination IP assay and a rescue experiment, we confirmed that CCNB1IP1 regulated the ubiquitination and degradation of cyclin B1. Combined with information from transcription factor database and AdipoR1 transcriptome sequencing, these results showed that estrogen receptor 1 (ESR1) may be a transcription factor of CCNB1IP1. We found that AdipoR1 promoted the translocation of ESR1 from the cytoplasm to the nucleus, and ESR1 inhibited the transcription of CCNB1IP1.Therefore, we propose that AdipoR1 regulates the ubiquitination level, cell cycle progression, and radiation resistance of HCC cells through the “AdipoR1 /ESR1/CCNB1IP1/cyclin B1” axis. This study will promote the development of novel targeted radiosensitizing drugs.

Radiotherapy is one of the main treatment modalities for advanced hepatocellular carcinoma (HCC). Ferroptosis has been shown to promote the radiosensitivity of HCC cells, but it remains unclear whether epigenetic regulations function in this process. In this study, we found that the overexpression of METTL3 was associated with poor prognosis. Knockdown of METTL3 promoted radiosensitivity of HCC by inducing ferroptosis. Mechanistically, METTL3 targeted adenine (+1795) on the SLC7A11 mRNA, and the m6A reader IGF2BP2 promoted SLC7A11 mRNA stability by recognizing and binding to the m6A site. Additionally, METTL3 decreased the ubiquitination of SLC7A11 protein through the m6A/YTHDF2/SOCS2 axis. Furthermore, in vivo studies showed that HCC models with low METTL3/IGF2BP2 expression have higher radiosensitivity. In conclusion, our study suggests that METTL3 regulates the stability of SLC7A11 mRNA in an m6A/IGF2BP2-dependent manner and the ubiquitination of SLC7A11 protein through the m6A/YTHDF2/SOCS2 pathway, both of which require the m6A methyltransferase activity of METTL3. METTL3 or IGF2BP2 may be promising targets for radiotherapy of HCC.

Among the spectrum of digestive system cancers, hepatocellular carcinoma (HCC) poses a particularly formidable challenge due to its poor prognosis. Geniposide, an iridoid glucoside extracted from the fruit of Gardenia jasminoides Ellis, exhibits a diverse array of biological activities. The goal of this study is to delineate the specific roles and underlying mechanisms of geniposide on the progression of HCC. Cell viability, apoptosis and migration of Huh7 and HepG2 cells were, respectively, assessed via CCK-8, flow cytometry and trans-well assays. The level of reactive oxygen species (ROS) was assessed with a dihydroethidium (DHE) probe. The measurement of mitochondrial membrane potential (MMP) was conducted using JC-1 staining. Ferroptosis-related markers were evaluated by Western Blot assay. Transcriptome sequencing was performed in HCC cells both treated and untreated with geniposide. In vivo experiments were applied with the subcutaneous xenograft tumor model. In vitro experiments revealed that geniposide exerted a concentration-dependent suppression on cell viability and migration, concurrently eliciting apoptosis in HCC cells. Ferroptosis was identified as the main form of geniposide-induced cell death in HCC. Geniposide promoted the iron ions levels, ROS accumulation, and the expression of ferroptosis markers, which were partially reversed by the addition of deferoxamine (DFO, ferroptosis inhibitor). Intersection analysis was applied between upregulated genes of HCC cells and ferroptosis-related genes. DUOX1 was proven to be involved in geniposide-mediated roles in HCC. In vivo experiments further clarified the suppressive effects of geniposide on tumors. Geniposide treatment increased intracellular iron ions and induced ferroptosis in HCC. Geniposide attenuated tumor progression and oxidative stress via DUOX1-mediated ferroptosis.

Ionizing radiation (IR) is a ubiquitous environmental radiation factor with natural and anthropogenic sources. The cumulative discharge of nuclear contaminated water into the ocean by Japan in the recent years has been making the impact of IR on aquatic living organisms a topic of great concern in both academic circles and public opinion. However, sex-specific mechanisms of IR-induced reproductive and offspring developmental toxicity remain poorly understood. Here, we investigated the sexually dimorphic effects of acute X-ray radiation on zebrafish (Danio rerio) reproduction using integrated phenotypic and molecular approaches. Transcriptome analysis revealed striking sexual dimorphism in radiation response, with male gonads showing extensive perturbation compared to female tissues. Female gonads exhibited coordinated protective responses characterized by enhanced immune system activation and membrane integrity maintenance, while male tissues showed significant disruption of iron homeostasis and oxidative stress pathways, particularly in ferroptosis-related genes. Paternal radiation induced more severe reproductive impairment compared to the maternal, as evidenced by reduced egg production and fertilization rates. Using transgenic zebrafish lines, we demonstrated that paternal predominantly drove developmental abnormalities in offspring, including vascular defects, increased immune cell infiltration, and neurological malformations. Radiation specifically damaged sperm morphology and motility. Compared to the ovaries, the testes suffered more severe oxidative damage and stress regulation issues, leading to more significant reproductive developmental disorders. Our findings provide molecular mechanistic evidence for sex-specific radiation sensitivity in aquatic organisms and highlight the importance of considering sexual dimorphism in radiation protection strategies.

Respiratory coronaviruses pose significant health threats to both humans and animals. Porcine respiratory coronavirus (PRCV) typically causes mild respiratory infections in pigs and serves as a valuable model for human respiratory coronavirus. However, the investigation of PRCV pathogenesis remains limited. This study investigates the prevalence, genetic diversity, and pathogenesis of PRCV in China. From 2022 to 2024, 1186 pig tracheal samples were collected across 10 provinces, revealing a widespread presence of PRCV with an 11.8 % overall prevalence. For the first time, we isolated a PRCV strain from China, designated PRCV/NM, which is closely related to American lineages. Notably, PRCV/NM demonstrated a strong tropism for respiratory epithelial cells and organoids, with no significant infection of intestinal tissues. Experimental infections in piglets revealed that PRCV/NM induces asymptomatic infections, accompanied by minimal pulmonary pathology and no intestinal involvement. Our study provides insights into the molecular epidemiology and pathogenesis of PRCV in China.

ObjectiveMost cases of hepatocellular carcinoma (HCC) arise as a consequence of cirrhosis. In this study, our objective is to construct a comprehensive diagnostic model that investigates the diagnostic markers distinguishing between cirrhosis and HCC.MethodsBased on multiple GEO datasets containing cirrhosis and HCC samples, we used lasso regression, random forest (RF)-recursive feature elimination (RFE) and receiver operator characteristic analysis to screen for characteristic genes. Subsequently, we integrated these genes into a multivariable logistic regression model and validated the linear prediction scores in both training and validation cohorts. The ssGSEA algorithm was used to estimate the fraction of infiltrating immune cells in the samples. Finally, molecular typing for patients with cirrhosis was performed using the CCP algorithm.ResultsThe study identified 137 differentially expressed genes (DEGs) and selected five significant genes (CXCL14, CAP2, FCN2, CCBE1 and UBE2C) to construct a diagnostic model. In both the training and validation cohorts, the model exhibited an area under the curve (AUC) greater than 0.9 and a kappa value of approximately 0.9. Additionally, the calibration curve demonstrated excellent concordance between observed and predicted incidence rates. Comparatively, HCC displayed overall downregulation of infiltrating immune cells compared to cirrhosis. Notably, CCBE1 showed strong correlations with the tumour immune microenvironment as well as genes associated with cell death and cellular ageing processes. Furthermore, cirrhosis subtypes with high linear predictive scores were enriched in multiple cancer-related pathways.ConclusionIn conclusion, we successfully identified diagnostic markers distinguishing between cirrhosis and hepatocellular carcinoma and developed a novel diagnostic model for discriminating the two conditions. CCBE1 might exert a pivotal role in regulating the tumour microenvironment, cell death and senescence.

Cell death maintains cell morphology and homeostasis during development by removing damaged or obsolete cells. The concentration of metal ions whithin cells is regulated by various intracellular transporters and repositories to maintain dynamic balance. External or internal stimuli might increase the concentration of metal ions, which results in ions overloading. Abnormal accumulation of large amounts of metal ions can lead to disruption of various signaling in the cell, which in turn can produce toxic effects and lead to the occurrence of different types of cell deaths. In order to further study the occurrence and development of metal ions overloading induced cell death, this paper reviewed the regulation of Ca2+, Fe3+, Cu2+ and Zn2+ metal ions, and the internal mechanism of cell death induced by overloading. Furthermore, we found that different metal ions possess a synergistic and competitive relationship in the regulation of cell death. And the enhanced level of oxidative stress was present in all the processes of cell death due to metal ions overloading, which possibly due to the combination of factors. Therefore, this review offers a theoretical foundation for the investigation of the toxic effects of metal ions, and presents innovative insights for targeted regulation and therapeutic intervention. • Metal ions overloading disrupts homeostasis, which in turn affects the regulation of cell death. • Metal ions overloading can cause cell death via reactive oxygen species (ROS). • Different metal ions have synergistic and competitive relationships for regulating cell death.

Radiation liver injury is a common complication of hepatocellular carcinoma radiotherapy. It is mainly caused by irreversible damage to the DNA of hepatocellular cells directly by radiation, which seriously interferes with metabolism and causes cell death. AdipoRon can maintain lipid metabolism and stabilize blood sugar by activating adiponectin receptor 1 (AdipoR1). However, the role of AdipoRon/AdipoR1 in the regulation of ionizing radiation (IR)-induced mitochondrial damage remains unclear. In this study, we aimed to elucidate the roles of AdipoRon/AdipoR1 in IR-induced mitochondrial damage in normal hepatocyte cells. We found that AdipoRon treatment rescued IR-induced liver damage in mice and mitochondrial damage in normal hepatocytes in vivo and in vitro. AdipoR1 deficiency exacerbated IR-induced oxidative stress, mitochondrial dynamics, and biogenesis disorder. Mechanistically, the absence of AdipoR1 inhibits the activity of adenosine monophosphate-activated protein kinase α (AMPKα), subsequently leading to disrupted mitochondrial dynamics by decreasing mitofusin (MFN) and increasing dynamin-related protein 1 (DRP1) protein expression. It also controls mitochondrial biogenesis by suppressing the peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) and transcription factor A (TFAM) signaling pathway, ultimately resulting in impaired mitochondrial function. To sum up, AdipoRon/AdipoR1 maintain mitochondrial function by regulating mitochondrial dynamics and biogenesis through the AdipoR1-AMPKα signaling pathway. This study reveals the significant role of AdipoR1 in regulating IR-induced mitochondrial damage in hepatocytes and offers a novel approach to protecting against damage caused by IR.

Background and aims: Radiotherapy is widely applied for lung adenocarcinoma (LUAD), while individualized differences led to different outcomes. This study aimed to establish a multi-gene risk scoring model to predict the benefits of LUAD patients from radiotherapy, based on different types of cell death respectively. Results: Other than autophagy, pyroptosis, ferroptosis and Immunogenic cell death (ICD), the LUAD prognostic model based on apoptosis had the best performance, and the area under curves (AUCs) of the receiver operating curve (ROC) for 1-, 3-, and 5-year OS were 0.700,0.736,0.723,respectively. Such genes were involved as SLC7A5, EXO1, ABAT, NLRP1 and GAR1. Then patients were divided into high and low risk groups by the median apoptosis-LUAD risk score. For patients in the high-risk group, i.e., the radiotherapy-tolerant group, we screened adjuvant chemotherapy and found that besides the conventional first-line chemotherapy regimen, drugs such as Fludarabine, Pevonedistat, and Podophyllotoxin Bromide may also have potential therapeutic value. Conclusion: The multi-gene risk scoring model based on apoptosis might predict the radiotherapy benefits of LUAD patients and for those radioresistant patients classified by the model we also provided effective adjuvant chemicals, which would be used to guide clinical treatment.

OBJECTIVE:The cardiovascular system effects of environmental low-dose radiation exposure on radiation practitioners remain uncertain and require further investigation. The aim of this study was to initially investigate and explore the mechanisms by which low-dose radiation may contribute to atherosclerosis through a multi-omics joint comprehensive basic experiment. METHODS:We used WGCNA and differential analyses to identify shared genes and potential pathways between radiation injury and atherosclerosis sequencing datasets, as well as tissue transcriptome immune infiltration level extrapolation and single-cell transcriptome data correction using the CIBERSORT deconvolution algorithm. Animal models were constructed by combining a high-fat diet with 5 Gy γ-ray whole-body low-dose ionizing radiation. The detection of NETs release was validated by enzyme-linked immunosorbent assay. RESULTS:Analysis reveals shared genes in both datasets of post-irradiation and atherosclerosis, suggesting that immune system neutrophils may be a key node connecting radiation to atherosclerosis. NETs released by neutrophil death can influence the development of atherosclerosis. Animal experiments showed that the number of neutrophils decreased (P < 0.05) and the concentration of NETs reduced after low-dose radiation compared with the control group, and the concentration of NETs significantly increased (P < 0.05) in the HF group. Endothelial plaques were significantly increased in the high-fat feed group and significantly decreased in the low-dose radiation group compared with the control group. CONCLUSIONS:Long-term low-dose ionizing radiation exposure stimulates neutrophils and inhibits their production of NETs, resulting in inhibition of atherosclerosis.

Highly efficient nanocomposites, hydrophobic molecularly imprinted magnetic covalent organic frameworks (MI-MCOF), have been farbricated by a facile Schiff-base reaction. The MI-MCOF was based on terephthalaldehyde (TPA) and 1,3,5-tris(4-aminophenyl) benzene (TAPB) as functional monomer and crosslinker, anhydrous acetic acid as catalyst, bisphenol AF as dummy template, and NiFe2O4 as magnetic core. This organic framework significantly reduced the time consumption of conventional imprinted polymerization and avoided the use of traditional initiator and cross-linking agents. The synthesized MI-MCOF exhibited superior magnetic responsivity and affinity, as well as high selectivity and kinetics for bisphenol A (BPA) in water and urine samples. The equilibrium adsorption capacity (Qe) of BPA on the MI-MCOF was 50.65 mg g−1, which was 3–7-fold higher than of its three structural analogues. The imprinting factor of BPA reached up to 3.17, and the selective coefficients of three analogues were all > 2.0, evidencing the excellent selectivity of fabricated nanocomposites to BPA. Based on the MI-MCOF nanocomposites, the magnetic solid-phase extraction (MSPE), combined with HPLC and fluorescence detection (HPLC-FLD), offered superior analytical performance: wide linear range of 0.1–100 μg L−1, high correlation coefficient of 0.9996, low limit of detection of 0.020 μg L−1, good recoveries of 83.5–110

PDF file - 207K, miR-133a exerted inhibitory effects on p53 mutant cell lines DLD1 and HT29.

Radiation-induced lung injury (RILI), divided into early radiation pneumonia (RP) and late radiation-induced pulmonary fibrosis (RIPF), is a common serious disease after clinical chest radiotherapy or nuclear accident, which seriously threatens the life safety of patients. There has been no effective prevention or treatment strategy till now. Epithelial-mesenchymal transition (EMT) is a key step in the occurrence and development of RILI. In this study, we demonstrated that emetine dihydrochloride (EDD) alleviated RILI through inhibiting EMT. We found that EDD significantly attenuated EMT-related markers, reduced Smad3 phosphorylation expression after radiation. Then, for the first time, we observed EDD alleviated lung hyperaemia and reduced collagen deposit induced by irradiation, providing protection against RILI. Finally, it was found that EDD inhibited radiation-induced EMT in lung tissues. Our study suggested that EDD alleviated RILI through inhibiting EMT by blocking Smad3 signalling pathways. In summary, our results indicated that EDD is a novel potential radioprotector for RILI.

A series of physiological and pathological changes occur after radiotherapy and accidental exposure to ionizing radiation (IR). These changes cause serious damage to human tissues and can lead to death. Radioprotective countermeasures are radioprotective agents that prevent and reduce IR injury or have therapeutic effects. Based on a good understanding of radiobiology, a number of protective agents have achieved positive results in early clinical trials. The present review grouped known radioprotective agents according to biochemical categories and potential clinical use, and reviewed radiation countermeasures, i.e., radioprotectors, radiation mitigators and radiotherapeutic agents, with an emphasis on their current status and research progress. The aim of the present review is to facilitate the selection and application of suitable radioprotectors for clinicians and researchers, to prevent or reduce IR injury.

As one of novel hallmarks of cancer, lipid metabolic reprogramming has recently been becoming fascinating and widely studied. Lipid metabolic reprogramming in cancer is shown to support carcinogenesis, progression, distal metastasis, and chemotherapy resistance by generating ATP, biosynthesizing macromolecules, and maintaining appropriate redox status. Notably, increasing evidence confirms that lipid metabolic reprogramming is under the control of dysregulated non-coding RNAs in cancer, especially lncRNAs and circRNAs. This review highlights the present research findings on the aberrantly expressed lncRNAs and circRNAs involved in the lipid metabolic reprogramming of cancer. Emphasis is placed on their regulatory targets in lipid metabolic reprogramming and associated mechanisms, including the clinical relevance in cancer through lipid metabolism modulation. Such insights will be pivotal in identifying new theranostic targets and treatment strategies for cancer patients afflicted with lipid metabolic reprogramming.