Carbon nanomaterials are some of the state-of-the-art materials used in drug-delivery and tissue-engineering research. Compared with traditional materials, carbon nanomaterials have the advantages of large specific surface areas and unique properties and are more suitable for use in drug delivery and tissue engineering after modification. Their characteristics, such as high drug loading and tissue loading, good biocompatibility, good targeting and long duration of action, indicate their great development potential for biomedical applications. In this paper, the synthesis and application of carbon dots (CDs), carbon nanotubes (CNTs) and graphene in drug delivery and tissue engineering are reviewed in detail. In this review, we discuss the current research focus and existing problems of carbon nanomaterials in order to provide a reference for the safe and effective application of carbon nanomaterials in drug delivery and tissue engineering.

The aberrant expression of sialyltransferase has a role in cell differentiation, neoplastic transformation and the progression of various types of cancer. Our previous studies have shown that high expression of β-galactoside-α2,3-sialyltransferase III (ST3Gal3) in the metastatic ovarian cancer cell line HO8910PM attenuated cisplatin-induced apoptosis. The present study demonstrated that paclitaxel-induced chemoresistance in ovarian cancer cells upregulated the expression of ST3Gal3 and reduced the activity of caspase-8/3. The results of the present study revealed that the endogenous levels of ST3Gal3 mRNA and protein were significantly higher in HO8910PM cells compared with SKOV3 cells. A higher expression of ST3Gal3 was correlated with an increased resistance to paclitaxel, while the downregulation of ST3Gal3 resulted in paclitaxel-induced apoptosis. Paclitaxel upregulated ST3Gal3 expression at the mRNA and protein levels in HO8910PM cells, but not in SKOV3 cells. Silencing of ST3Gal3 by small interfering RNA reversed these effects and increased the protein levels of caspase-8/3, which may contribute to paclitaxel-induced apoptosis. The results of the present study suggested that ST3Gal3 was a target for paclitaxel-related resistance during ovarian cancer chemotherapy.

Purpose Aims to compare the prognostic performance of the number of positive lymph nodes (PLNN), lymph node ratio (LNR) and log odds of metastatic lymph nodes (LODDS) and establish a prognostic nomogram to predict overall survival (OS) rate for patients with endometrial carcinosarcoma (ECS). Methods Patients were retrospectively obtained from Surveillance, Epidemiology and End Results (SEER) database from 2004 to 2015. The prognostic value of PLNN, LNR and LODDS were assessed. A prediction model for OS was established based on univariate and multivariate analysis of clinical and demographic characteristics of ECS patients. The clinical practical usefulness of the prediction model was valued by decision curve analysis (DCA) through quantifying its net benefits. Results The OS prediction accuracy of LODDS for ECS is better than that of PLNN and LNR. Five factors, age, tumor size, 2009 FIGO, LODDS and peritoneal cytology, were independent prognostic factors of OS. The C-index of the nomogram was 0.743 in the training cohort. The AUCs were 0.740, 0.682 and 0.660 for predicting 1-, 3- and 5-year OS, respectively. The calibration plots and DCA showed good clinical applicability of the nomogram, which is better than 2009 FIGO staging system. These results were verified in the validation cohort. A risk classification system was built that could classify ECS patients into three risk groups. The Kaplan-Meier curves showed that OS in the different groups was accurately differentiated by the risk classification system and performed much better than FIGO 2009. Conclusion Our results indicated that LODDS was an independent prognostic indicator for ECS patients, with better predictive efficiency than PLNN and LNR. A novel prognostic nomogram for predicting the OS rate of ECS patients was established based on the population in the SEER database. Our nomogram based on LODDS has a more accurate and convenient value for predicting the OS of ECS patients than the FIGO staging system alone.

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Cervical cancer is one of the most common malignant tumors in women. Circular RNA (circRNA) has been shown to play a crucial role in cervical cancer. Here, the aim of this study was to explore the functions and a novel miRNA/mRNA network underlying circ_0000212 in cervical cancer regulation. The expression of circ_000212, miR-625-5p and Protein Tyrosine Phosphatase 4A1 (PTP4A1) mRNA was measured by quantitative real-time PCR (qRT-PCR). 5-ethynyl-2’-deoxyuridine assay was conducted to detect the proliferation of cervical cancer cells. Wound healing and transwell assays were employed to assess cell migration and invasion. The angiogenesis abilities of cervical cancer cells were evaluated by tube formation assay. Flow cytometry was performed for analyzing cell apoptosis. The expression of PTP4A1 protein and apoptosis-relative protein were detected via western blot. The dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were employed to clarify the interaction between circ_0000212 or PTP4A1 and miR-625-5p. The impact of circ_0000212 on cervical cancer growth in vivo was detected by xenograft assay. Circ_0000212 and PTP4A1 were highly expressed and miR-625-5p expression level was decreased in cervical cancer. Circ_0000212 silencing suppressed cervical cancer cell proliferation, migration, invasion and angiogenesis while promoting apoptosis. MiR-625-5p was targeted by circ_0000212, and miR-625-5p inhibition reversed the effects of circ_0000212 knockdown. MiR-625-5p directly targeted PTP4A1, and the inhibitory effect of miR-625-5p on the malignant progression of cervical cancer was reversed after PTP4A1 overexpression. In-vivo assays validated that circ_0000212 promoted cervical cancer tumor growth in vivo. circ_0000212 acted as an oncogene in cervical cancer progression, and knockdown of circ_0000212 repressed cervical cancer development by increasing miR-625-5p and decreasing PTP4A1.