As an essential trace element in the human body, transitional metal copper (Cu) ions are the bioactive components within the body featuring dedicated biological effects such as promoting angiogenesis and influencing lipid/glucose metabolism. The recent substantial advances of nanotechnology and nanomedicine promote the emerging of distinctive Cu‐involved biomaterial nanoplatforms with intriguing theranostic performances in biomedicine, which are originated from the biological effects of Cu species and the physiochemical attributes of Cu‐composed nanoparticles. Based on the very‐recent significant progresses of Cu‐involved nanotheranostics, this work highlights and discusses the principles, progresses, and prospects on the elaborate design and rational construction of Cu‐composed functional nanoplatforms for a diverse array of biomedical applications, including photonic nanomedicine, catalytic nanotherapeutics, antibacteria, accelerated tissue regeneration, and bioimaging. The engineering of Cu‐based nanocomposites for synergistic nanotherapeutics is also exemplified, followed by revealing their intrinsic biological effects and biosafety for revolutionizing their clinical translation. Finally, the underlying critical concerns, unresolved hurdles, and future prospects on their clinical uses are analyzed and an outlook is provided. By entering the “Copper Age,” these Cu‐involved nanotherapeutic modalities are expected to find more broad biomedical applications in preclinical and clinical phases, despite the current research and developments still being in infancy.

• Ultrasound is a useful tool in percutaneous laser ablation (PLA). • PLA is safe for treating papillary thyroid microcarcinoma. • PLA is effective for single papillary thyroid microcarcinoma.

Purpose SIK2 is a centrosome kinase required for mitotic spindle formation and a potential target for ovarian cancer therapy. Here we examine the effects of a novel small molecule SIK2 inhibitor, ARN-3236, on sensitivity to paclitaxel in ovarian cancer. Experimental Design SIK2 expression was determined in ovarian cancer tissue samples and cell lines. ARN-3236 was tested for its efficiency to inhibit growth and enhance paclitaxel sensitivity in cultures and xenografts of ovarian cancer cell lines. SIK2 siRNA and ARN-3236 were compared for their ability to produce nuclear-centrosome dissociation, inhibit centrosome splitting, block mitotic progression, induce tetraploidy, trigger apoptotic cell death and reduce AKT/survivin signaling. Results SIK2 is overexpressed in approximately 30% of high grade serous ovarian cancers. ARN-3236 inhibited growth of 10 ovarian cancer cell lines at an IC50 of 0.8 to 2.6 μM, where the IC50 of ARN-3236 was inversely correlated with endogenous SIK2 expression (Pearson’s r = −0.642, P = 0.03). ARN-3236 enhanced sensitivity to paclitaxel in 8 of 10 cell lines, as well as in SKOv3ip (P = 0.028) and OVCAR8 xenografts. In at least three cell lines a synergistic interaction was observed. ARN-3236 uncoupled the centrosome from the nucleus in interphase, blocked centrosome separation in mitosis, caused prometaphase arrest and induced apoptotic cell death and tetraploidy. ARN-3236 also inhibited AKT phosphorylation and attenuated survivin expression. Conclusions ARN-3236 is the first orally available inhibitor of SIK2 to be evaluated against ovarian cancer in preclinical models and shows promise in inhibiting ovarian cancer growth and enhancing paclitaxel chemosensitivity.

Three-dimensional nitrogen-doped graphene (3D N-doped graphene) was prepared through chemical vapor deposition (CVD) by using porous nickel foam as a substrate. As a model, a dopamine biosensor was constructed based on the 3D N-doped graphene porous foam. Electrochemical experiments exhibited that this biosensor had a remarkable detection ability with a wide linear detection range from 3 × 10(-6) M to 1 × 10(-4) M and a low detection limit of 1 nM. Moreover, the fabricated biosensor also showed an excellent anti-interference ability, reproducibility, and stability.

Cisplatin is commonly used in ovarian cancer chemotherapy, however, chemoresistance to cisplatin remains a great clinical challenge. Oncogenic transcriptional factor FOXM1 has been reported to be overexpressed in ovarian cancer. In this study, we aimed to investigate the potential role of FOXM1 in ovarian cancers with chemoresistance to cisplatin. Our results indicate that FOXM1 is upregulated in chemoresistant ovarian cancer samples, and defends ovarian cancer cells against cytotoxicity of cisplatin. FOXM1 facilitates DNA repair through regulating direct transcriptional target EXO1 to protect ovarian cancer cells from cisplatin-mediated apoptosis. Attenuating FOXM1 and EXO1 expression by small interfering RNA, augments the chemotherapy efficacy against ovarian cancer. Our findings indicate that targeting FOXM1 and its target gene EXO1 could improve cisplatin effect in ovarian cancer, confirming their role in modulating cisplatin sensitivity.

Epidermal growth factor receptor (EGFR) overexpression and activation result in increased proliferation and migration of solid tumors including ovarian cancer. In recent years, mounting evidence indicates that EGFR is a direct and functional target of miR-7. In this study, we found that miR-7 expression was significantly downregulated in highly metastatic epithelial ovarian cancer (EOC) cell lines and metastatic tissues, whereas the expression of, EGFR correlated positively with metastasis in both EOC patients and cell lines. Overexpression of miR-7 markedly suppressed the capacities of cell invasion and migration and resulted in morphological changes from a mesenchymal phenotype to an epithelial-like phenotype in EOC. In addition, overexpression of miR-7 upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, accompanied with EGFR inhibition and AKT/ERK1/2 inactivation. Similar to miR-7 transfection, silencing of EGFR with this siRNA in EOC cells also upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, and decreased phosphorylation of both Akt and ERK1/2, confirming that EGFR is a target of miR-7 in reversing EMT. The pharmacological inhibition of PI3K-AKT and ERK1/2 both significantly enhanced CK-18 and β-catenin expression and suppressed vimentin expression, indicating that AKT and ERK1/2 pathways are required for miR-7 mediating EMT. Finally, the expression of miR-7 and EGFR in primary EOC with matched metastasis tissues was explored. It was showed that miR-7 is inversely correlated with EGFR. Taken together, our results suggested that miR-7 inhibited tumor metastasis and reversed EMT through AKT and ERK1/2 pathway inactivation by reducing EGFR expression in EOC cell lines. Thus, miR-7 might be a potential prognostic marker and therapeutic target for ovarian cancer metastasis intervention.

As a non‐invasive treatment modality with high tissue‐penetration depth, ultrasound‐triggered sonodynamic therapy (SDT) has been extensively explored and is regarded as the alternative choice to overcome the drawbacks of conventional photo‐triggered therapies. Nevertheless, the low quantum yield of sonosensitizer, tumor hypoxia, and undesirable therapeutic efficiency are still the major concerns of SDT. It is highly challenging but necessary to explore the SDT‐based synergistic, augmented, and noninvasive therapeutic modalities. Herein, a distinct TiO2Fe3O4@PEG Janus nanostructure composed of the typical sonosensitizer TiO2 and nanoenzyme Fe3O4 is rationally designed and engineered for bilaterally enhanced SDT and chemodynamic therapy (CDT). The deposition of Fe3O4 component on the surface of TiO2 can not only endow the Janus nanosonosensitizers with Fenton‐catalytic activity to generate hydroxyl radicals (•OH) from tumor‐endogenous overexpressed H2O2 for CDT but also enhance the SDT performance of TiO2 via narrowing the band gap of TiO2 and reducing the recombination rate of the electrons (e–/h+) pair. In turn, the US activation can both accelerate mass transfer and chemical reaction rates of the Fenton reaction to enhance the CDT effect. The high efficacy of bilaterally enhanced SDT and CDT is systematically demonstrated both in vitro and in vivo.

Intraluminal stenting can prevent the formation of caustic esophageal stricture. The location of the cicatricial esophagus dictates whether to perform concomitant esophagectomy during esophageal reconstruction. Platysma myocutaneous flap repair is an excellent method for the treatment of severe cervical esophageal or anastomotic stricture.