Cancer ranks as the second leading cause of death worldwide, causing a large social and economic burden. However, most anti-cancer treatments face the problems of tumor recurrence and metastasis. Therefore, finding an effective cure for cancer needs to be solved urgently. Recently, the discovery of cancer stem cells (CSCs) provides a new orientation for cancer research and therapy. CSCs share main characteristics with stem cells and are able to generate an entire tumor. Besides, CSCs usually escape from current anti-cancer therapies, which is partly responsible for tumor recurrence and poor prognosis. microRNAs (miRNAs) belong to small noncoding RNA and regulate gene post-transcriptional expression. The dysregulation of miRNAs leads to plenty of diseases, including cancer. The aberrant miRNA expression in CSCs enhances stemness maintenance. In this review, we summarize the role of miRNAs on CSCs in the eight most common cancers, hoping to bridge the research of miRNAs and CSCs with clinical applications. We found that miRNAs can act as tumor promoter or suppressor. The dysregulation of miRNAs enhances cell stemness and contributes to tumor metastasis and therapeutic resistance via the formation of feedback loops and constitutive activation of carcinogenic signaling pathways. More importantly, some miRNAs may be potential targets for diagnosis, prognosis, and cancer treatments.

Breast cancer is the most common malignant tumors in females. Although the conventional treatment has demonstrated a certain effect, some limitations still exist. The Rho guanosine triphosphatase (GTPase) Cdc42 (Cell division control protein 42 homolog) is often upregulated by some cell surface receptors and oncogenes in breast cancer. Cdc42 switches from inactive guanosine diphosphate (GDP)-bound to active GTP-bound though guanine-nucleotide-exchange factors (GEFs), results in activation of signaling cascades that regulate various cellular processes such as cytoskeletal changes, proliferation and polarity establishment. Targeting Cdc42 also provides a strategy for precise breast cancer therapy. In addition, Cdc42 is a potential target for several types of non-coding RNAs including microRNAs and lncRNAs. These non-coding RNAs is extensively involved in Cdc42-induced tumor processes, while many of them are aberrantly expressed. Here, we focus on the role of Cdc42 in cell morphogenesis, proliferation, motility, angiogenesis and survival, introduce the Cdc42-targeted non-coding RNAs, as well as present current development of effective Cdc42-targeted inhibitors in breast cancer.

Cancer, as the second leading cause of death worldwide, is a major public health concern that imposes a heavy social and economic burden. Effective approaches for either diagnosis or therapy of most cancers are still lacking. Dynamic monitoring and personalized therapy are the main directions for cancer research. Cancer-derived extracellular vesicles (EVs) are potential disease biomarkers. Cancer EVs, including small EVs (sEVs), contain unique biomolecules (protein, nucleic acid, and lipids) at various stages of carcinogenesis. In this review, we discuss the biogenesis of sEVs, and their functions in cancer, revealing the potential applications of sEVs as cancer biomarkers.

Aims: Chronic cerebral hypoperfusion drives the progression of intracranial atherosclerotic stenosis (ICAS) and increases ischemic risk. Endothelial angiogenic adaptation initially preserves cerebral perfusion but deteriorates with disease progression. We investigated whether the HCG11/QKI5 axis represents a regulatory node with therapeutic potential in cerebral hypoperfusion. Methods: Circulating hypoxia‐ and angiogenesis‐related biomarkers were compared between asymptomatic and symptomatic ICAS patients to reflect different progression stages. Endothelial function was assessed in oxygen–glucose deprivation models following HCG11 overexpression or QKI5 knockdown. A rat model of chronic cerebral hypoperfusion was used to evaluate temporal changes in vivo. Results: Pro‐angiogenic factors were elevated in asymptomatic ICAS but reduced in symptomatic patients, indicating progressive impairment of vascular compensation. HCG11 overexpression enhanced endothelial proliferation and tube formation, whereas QKI5 silencing attenuated these responses. These effects were associated with modulation of HIF‐1α/VEGF signaling. In vivo, early hypoperfusion activated QKI5 and angiogenic pathways, followed by a gradual decline during sustained hypoperfusion. Conclusion: Progressive attenuation of the HCG11/QKI5‐mediated angiogenic program may underlie endothelial adaptive failure in cerebral hypoperfusion. Targeting this RNA‐regulatory axis may represent a potential therapeutic strategy to preserve vascular compensation and mitigate disease progression in ICAS.

BACKGROUND: Tenecteplase improves reperfusion and functional outcomes compared with alteplase in patients with large vessel occlusion. We assessed whether this superiority varies with thrombolysis-to-puncture time (TTP). METHODS: This retrospective analysis of a prospective multicenter cohort included patients with large vessel occlusion who received bridging therapy with either tenecteplase or alteplase between January 2022 and September 2025. Patients were stratified by TTP (<60 versus ≥60 minutes). We subsequently assessed the association of TTP with efficacy and safety outcomes between the alteplase and tenecteplase groups using multivariable logistic regression adjusted for age, baseline National Institutes of Health Stroke Scale score, and time from stroke onset to arterial puncture. Functional independence was defined as a modified Rankin Scale score of 0 to 2 at 3 months. RESULTS: Of 1106 patients who received bridging therapy, 1003 were included in the primary analysis (tenecteplase, 488; alteplase, 515). The median age was 68 (interquartile range, 58–75) years in both groups, with men comprising 64.3% and 66.0%, respectively. Tenecteplase was associated with superior 3-month functional independence compared with alteplase (53.6% versus 48.1%; adjusted odds ratio, 1.37 [95% CI, 1.03–1.82]). This benefit was concentrated in patients with a TTP <60 minutes, where tenecteplase yielded higher rates of both early recanalization (19.0% versus 9.1%; adjusted odds ratio, 2.36 [95% CI, 1.32–4.23]; P _interaction =0.047) and functional independence (61.0% versus 49.0%; adjusted odds ratio, 1.77 [95% CI, 1.13–2.77]; P _interaction =0.111). No between-agent differences were significant with TTP ≥60 minutes. Safety outcomes were comparable, but each 30-minute TTP increase independently elevated hemorrhagic risks for both agents. CONCLUSIONS: The recanalization superiority of tenecteplase over alteplase is time-dependent, evident only within a TTP <60 minutes. Although the translation of this advantage into functional outcome was not statistically modified by time, optimizing workflow to achieve this rapid window maximizes the potential benefit of tenecteplase, which should be prioritized in capable settings.