Cancer stem cells (CSCs) have been reported to play critical roles in tumor initiation, propagation, and regeneration of cancer. Nano-size vehicles are employed to deliver drugs to target the CSCs for cancer therapy. Polymeric nanoparticles have been considered as the most efficient vehicles for drug delivery due to their excellent pharmacokinetic properties. The CSCs specific antibodies or ligands can be conjugated onto the surface or interior of nanoparticles to successfully target and finally eliminate CSCs. In this review, we focus on the approaches of polymeric nanoparticles design for loading drug, and their potential application for CSCs targeting in cancer therapy.

The theory of cancer stem-like cell (or cancer stem cell, CSC) has been established to explain how tumor heterogeneity arises and contributes to tumor progression in diverse cancer types. CSCs are believed to drive tumor growth and elicit resistance to conventional therapeutics. Therefore, CSCs are becoming novel target in both medical researches and clinical studies. Emerging evidences showed that nanoparticles effectively inhibit many types of CSCs by targeting various specific markers (aldehyde dehydrogenases, CD44, CD90, and CD133) and signaling pathways (Notch, Hedgehog, and TGF-β), which are critically involved in CSC function and maintenance. In this review, we briefly summarize the current status of CSC research and review a number of stateof-the-art nanomedicine approaches targeting CSC. In addition, we discuss emerging therapeutic strategies using epigenetic drugs to eliminate CSCs and inhibit cancer cell reprogramming.

Renal cell carcinoma (RCC) is a common form of urologic tumor that originates from the highly heterogeneous epithelium of renal tubules. Over the last decade, targeting therapies to renal cancer cells have transformed clinical care for RCC. Recently, it was proposed that renal cancer stem cells (CSCs) isolated from renal carcinomas were responsible for driving tumor growth and resistance to conventional chemotherapy and radiotherapy, according to the theory of CSCs; this has provided the rationale for therapies targeting this aggressive cell population. Precise identification of renal CSC populations and the complete cell hierarchy will accurately inform characterization of disease subtypes. This will ultimately contribute to more personalized and targeted therapies. Here, we summarize potential targeting strategies for renal cancer cells and renal CSCs, including tyrosine kinase inhibitors, mammalian target of rapamycin inhibitors (mTOR), interleukins, CSC marker inhibitors, bone morphogenetic protein-2, antibody drug conjugates, and nanomedicine. In conclusion, targeting therapies for RCC represent new directions for exploration and clinical investigation and they plant a seed of hope for advanced clinical care.

long non-coding rna (lncrna) cancer susceptibility candidate 2 (caSc2) has been reported to exert an important role in acute lung injury (ali). The present study aimed to investigate the potential underlying mechanism of caSc2 in ali progression. reverse transcription-quantitative Pcr was conducted to examine the expression of caSc2, microrna (mir/mirna)-27b and TGF-β activated kinase 1 and MaP3K7-binding protein 2 (TaB2) in a549 cells. cell viability and apoptosis were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. enzyme-linked immunosorbent assay was used to measure the levels of inflammatory-related cytokines to assess the inflammatory response, including interleukin-1β (il-1β), il-6 and tumor necrosis factor α (TnF-α). The binding sites of mir-27b in caSc2 or TaB2 were predicted using lncBase or microT-cdS software, following which dual-luciferase reporter and rna binding protein immunoprecipitation assays were performed to confirm the target relationship between mir-27b and caSc2 or TaB2. The protein expression of TaB2 was detected by western blotting. The decreased viability, and increased apoptosis and inflammatory responses were attenuated by the accumulation of caSc2 in lipopolysaccharide (lPS)-stimulated a549 cells. caSc2 could directly bind to mir-27b in a549 cells. caSc2 protected a549 cells from lPS-triggered injury by downregulating mir-27b. TAB2 was a target of miR-27b in A549 cells. The influence of mir-27b depletion was reversed by the silencing of TaB2 in an ali cell model. caSc2 could increase the expression of TaB2 by serving as a competing endogenous rna of mir-27b in a549 cells. collectively, the results suggested that caSc2 attenuated lPS-induced injury in the ali cell model by modulating the mir-27b/TaB2 axis.

Vesicles 107 ± 19 nm in diameter, based on the self-assembly of tetra-para-phosphonomethyl calix[4]- arene bearing n-hexyl moieties attached to the phenolic oxygen centres, are effective in binding carboplatin within the cavity of the macrocycle under shear induced within a dynamic thin film in a continuous flow vortex fluidic device. Post shearing the vesicles maintain similar diameters and retain carboplatin within the cavity of the calixarene in a hierarchical structure, with their size and morphology investigated using DLS, TEM, SEM and AFM. Location of the carboplatin was confirmed using NMR, FTIR, ESI-MS and EFTEM, with molecular modelling favouring the polar groups of carboplatin hydrogen bonded to phosphonic acid moieties and the four member cyclobutane ring directed into the cavity of the calixarene. The loading efficiency and release profile of carboplatin was investigated using LC-TOF/MS, with the high loading of the drug achieved under shear and preferential released at pH 5.5, offering scope for anti-cancer drug delivery. The hierarchical structured vesicles increase the efficacy of carboplatin by 4.5 fold on ovarian cancer cells, lowered the IC50 concentration by 10 fold, and markedly increased the percent of cells in the S-phase (DNA replication) of the cell cycle.