Most photodynamic therapy (PDT) paradigms work through the highly O2-dependent type II photoreaction to generate singlet oxygen (1O2). The hypoxic microenvironment of solid tumors severely hampers therapeutic outcomes. Here, we present a novel design that could transfer the photophysical and photochemical properties of traditional phthalocyanine-based photosensitizers from type II photoreaction to efficient type I photoreaction and vibrational relaxation-induced photothermal conversion. These features enable the obtained nanostructured phthalocyanine assemblies (e.g., NanoPcAF) to display excellent phototherapies under both normoxic and hypoxic conditions. Moreover, NanoPcAF has a high level of accumulation in tumor tissues after intravenous injection, and 94% of tumor growth is inhibited in a preclinical model at a NanoPcAF dose of 0.8 nmol g–1 and light dose of 300 J cm–2.

Background:The role of DGCR8 in VSMCs is not known. Results: Loss of DGCR8 in VSMCs results in embryonic mortality by inhibiting cell proliferation and differentiation and promoting apoptosis. Conclusion: DGCR8 is required for vascular development. Significance: Elucidation of the role of DGCR8 in VSMCs will reveal the significance of DGCR8-mediated miRNA maturation in vascular diseases.

Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.