Circular RNAs (circRNAs) are a group of non‐coding RNAs implicated in the pathogenesis of cancer progression, which exert their functions via regulation of microRNAs (miRNAs) and genes. The present study uses gain‐ and loss‐of‐function approaches to evaluate the functions of hsa_circRNA_002178 in angiogenesis along with energy metabolism and underlying downstream signals. The expression pattern of hsa_circRNA_002178 in clinical breast cancer tissues and its association with prognosis were characterized at first. Next, the energy metabolism and angiogenesis as well as cell viability were evaluated when the expression of hsa_circRNA_002178 in breast cancer cells was knocked down by siRNA. The interaction between hsa_circRNA_002178 and its downstream miR‐328‐3p was identified, followed by the analysis of their functions in regulation of breast cancer cellular behaviours. The target gene of miR‐328‐3p was predicted and verified, followed by identifying its role in the breast cancer progression. Higher expression of hsa_circRNA_002178 shared an association with worse prognosis in breast cancer. The inhibition of hsa_circRNA_002178 resulted in reductions in cell viability, energy metabolism and tube formation ability. Hsa_circRNA_002178 could competitively bind to miR‐328‐3p and down‐regulated its expression. Restoration of miR‐328‐3p eliminated the tumour‐promoting effects of hsa_circRNA_002178. COL1A1, as a target of miR‐328‐3p, could be up‐regulated by overexpression of hsa_circRNA_002178. In vivo experiments further confirmed the inhibition of tumour growth and inflammation by silencing hsa_circRNA_002178 or up‐regulating miR‐328‐3p. Taken together, hsa_circRNA_002178 is highlighted as a promising target for breast cancer due to the anti‐tumour effects achieved by silencing hsa_circRNA_002178.

Non-palpable breast cancer lesions pose a challenge for surgeons to resect cancer lesions. Making 'invisible' lesions 'visible' is the main strategy. Currently, multiple preoperative localization techniques have been applied in clinical. Among them, wire-guided localization (WGL) is the most common procedure due to its convenience and low cost. However, its limitations including discomfort, wire migration and the coupling of localization and operation procedures cause troubles for surgeons and patients. The desire for localization methods improvement, accompanied by the advance of emerging science and technology, leads to the development of a series of locating approaches for breast non-palpable lesions, aiming to improve locating accuracy while reducing adverse events. These emerging methods have undergone improvements from steel wire to functional particles, from radioactivity to non-radioactive, which help doctors and patients choose a more appropriate scheme. This review outlines the principles, procedures, advantages and disadvantages of these locating methods, and highlights the latest progress and related clinical data on innovative locating approaches. Finally, we briefly discuss the current challenges and future opportunities for the clinical application of these localization approaches.

Systemic chemotherapy and radiotherapy often yield poor effect in the postoperative treatment of non-small cell lung cancer (NSCLC) and induce drug resistance. Herein, we proposed a targeted therapeutic approach utilizing gene carrier-mediated specific shRNA method. Firstly, the targeted short hairpin shRNA sequence, designed based on the STAT3 gene sequence, was inserted into the eukaryotic expression vector pGPU6/GFP/Neo to form the recombinant plasmid STAT3-shRNA. Next, a novel gene carrier, Vitamin E Succinate-Chitosan-Histidine (VES-CTS-His, VCH), was synthesized through an acylation reaction. The VCH was combined with pGPU6/GFP/Neo STAT3-shRNA recombinant plasmid by electrostatic interactions to form stable particles. VCH/pDNA, with typical nanoscale dimensions, could accumulate in tumor tissues through the EPR effect and enter tumor cells via endocytosis. VCH exhibited good pH responsiveness and could dissociate in the acidic microenvironment of tumors, thereby releasing the plasmids. Subsequently, the plasmids could downregulate STAT3 expression through RNAi effect. Inhibiting or blocking the expression of the STAT3 gene could significantly enhance the apoptotic induction and growth inhibition effects on NSCLC cells through the PI3K and mTOR signaling pathways, thereby achieving the goal of tumor treatment. This study provides a novel method for the construction of novel non-viral gene carriers and clinical gene-targeted therapy for NSCLC.