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Background: At the pan-cancer level, exploring the expression and prognostic significance of a gene, such as UBE2S, will help to gain insight into the role of the gene and its feasibility for cancer screening, prognosis assessment and even gene therapy. Methods: The Cancer Genome Atlas, Human Protein Atlas, Kaplan–Meier, Tumor Immunology Estimation Resource and other databases were used to analyze the expression of UBE2S at the pan-cancer level, its prognosis and the role of the immune microenvironment. Immunohistochemistry samples of tumor tissue collected in our clinic were taken as verification. Results: UBE2S is significantly overexpressed in pan-cancer and is closely associated with malignant clinical features, poor prognosis and tumor-associated macrophages. Conclusion: UBE2S may be a potential diagnostic and prognostic marker for pan-cancer and is associated with tumor-associated macrophages. [ABSTRACT FROM AUTHOR]

In the past few years, platinum nanomaterials (Pt NMs) have gained attraction owing to their ability to address the drawbacks of classical Pt-based chemotherapy drugs including drug resistance and clinical side effects, which have been preliminarily used in lung cancer, liver cancer, gynecological cancer, etc. In order to investigate the effect of Pt NMs on hematopoietic tumors, ultra-small Pt nanoclusters (Pt NCs) were employed to clarify their targeting recognition, cellular uptake, and effective therapy in vivo for chronic myeloid leukemia (CML) cells. Through the facile surface modification of Pt NCs with anti-CD19 to form the anti-CD19-Pt NC composite, the specific aggregation in BV173 cells could be realized based on their high protein expression of CD19 in comparison to that in CD19-negative K562 cells. Furthermore, the endocytic pathways of Pt NCs in K562 and BV173 cells were investigated by qualitative and quantitative analyses via inductively coupled plasma-optical emission spectroscopy and flow cytometry. It was observed that Pt NCs entered into the K562 cells mainly through the caveolin-dependent endocytic pathway and in BV173 cells primarily via phagocytosis and micropinocytosis. Moreover, these Pt NCs exerted an excellent inhibitory effect on proliferation, migration, and invasion of hematopoietic tumor cells and tended to gather the acidic organelles (lysosomes or endosomes), resulting in the proliferation inhibition of tumor cells by the generation of corrosive Pt. Notably, Pt NCs were significantly aggregated at the site of tumor inoculation in mice and exhibited satisfactory in vivo inhibition of the increase in tumor weight and its size under the premise of not damaging the liver and spleen. Thus, the merits of versatile Pt NCs included facile target recognition, explicit cellular uptake behavior, and therapeutic efficacy in vivo, thereby hinting at their promising prospects for the clinical diagnosis and treatment of hematological malignancies. [ABSTRACT FROM AUTHOR]

According to the 2020 GLOBOCAN Global Cancer Women's Cancer Data, ovarian cancer is the eighth most common tumor in humans. Still, its mortality rate ranks first among all gynecological tumors, with a 5-year survival rate of 30% to 50%. Widespread clinical use of platinum-based drugs has improved survival outcomes in patients with ovarian cancer, but organ toxicity and drug resistance hinder their anticancer effects. In particular, the resistance to platinum drugs is an important reason for ovarian cancer's high recurrence rate and mortality. With the development of chemotherapeutic drugs synthesized by nanomaterials in the biomedical field, we developed bifunctional ultrafine polyethyleneimine caged platinum nanoclusters (PEI-Pt NCs) to improve the dilemma of platinum drugs. This study aimed to elucidate the antitumor effect of PEI-Pt NCs in OC. First, as observed by confocal microscopy, Pt NCs entered OC cells in a dose-dependent manner and accumulated on the surface of the nuclear membrane and in the nucleus. Subsequently, through cck8, ki-67 immunofluorescence, wound healing assay, transwell assay, clone formation assay, flow cytometry, tunel staining, and western blotting assay, it was confirmed that PEI-Pt NCs could inhibit the proliferation and migration and induce the apoptosis of ovarian cancer cells. PEI-Pt NCs can be used as fluorescent markers for systemic bioimaging of ovarian cancer, showing great potential in diagnosing and treating ovarian cancer, and making a specific contribution to solving the dilemma of platinum-based drug therapy for OC. [ABSTRACT FROM AUTHOR]

The contribution of type II alveolar epithelial stem cells (AEC II) to radiation-induced lung fibrosis (RILF) is largely unknown. Cell differentiation phenotypes are determined by the balance between Lin28 and lethal-7 microRNA (let-7 miRNA). Lin28 is activated by β-catenin. The aim of this study was to track AEC II phenotypes at different phases of injury following thoracic irradiation and examine the expression of β-catenin, Lin28 and let-7 to identify their role in AEC II differentiation. Results showed that coexpression of prosurfactant protein C (proSP-C, an AEC II biomarker) and HOPX (homeobox only protein X, an AEC I biomarker) or vimentin (a differentiation marker) was detected in AEC II post-irradiation. The protein expression levels of HOPX and proSP-C were significantly downregulated, but vimentin was significantly upregulated following irradiation. The expression of E-cadherin, which prevents β-catenin from translocating to the nucleus, was downregulated, and the expression of β-catenin and Lin28 was upregulated after irradiation (P  < 0.05 to P  < 0.001). Four let-7 miRNA members (a, b, c and d) were upregulated in irradiated lungs (P  < 0.05 to P  < 0.001), but let-7d was significantly downregulated at 5 and 6 months (P  < 0.001). The ratios of Lin28 to four let-7 members were low during the early phase of injury and were slightly higher after 2 months. Intriguingly, the Lin28/let-7d ratio was strikingly increased after 4 months. We concluded that β-catenin contributed to RILF by promoting Lin28 expression, which increased the number of AEC II and the transcription of profibrotic molecules. In this study, the downregulation of let-7d miRNA by Lin28 resulted in the inability of AEC II to differentiate into type I alveolar epithelial cells (AEC I). [ABSTRACT FROM AUTHOR]