Progress of engineered bacteria for tumour therapy.

Finding novel therapeutic modalities, improving drug delivery efficiency and targeting, and reducing the immune escape of tumor cells are currently hot topics in the field of tumor therapy. Bacterial therapeutics have proven highly effective in preventing tumor spread and recurrence, used alone or in combination with traditional therapies. In recent years, a growing number of researchers have significantly improved the targeting and penetration of bacteria by using genetic engineering technology, which has received widespread attention in the field of tumor therapy. In this paper, we provide an overview and assessment of the advancements made in the field of tumor therapy using genetically engineered bacteria. We cover three major aspects: the development of engineered bacteria, their integration with other therapeutic techniques, and the current state of clinical trials. Lastly, we discuss the limitations and challenges that are currently being faced in the utilization of engineered bacteria for tumor therapy.

The role and molecular mechanism of NOP16 in the pathogenesis of nasopharyngeal carcinoma.

We aimed to explore the effects of NOP16 on the pathogenesis of nasopharyngeal carcinoma (NPC) and the related mechanism. In this study, the expression level of NOP16 in NPC tissues and adjacent tissues was measured by qRT-polymerase chain reaction (PCR) and immunohistochemistry (IHC) tests. In the in vitro study, the expression levels of NOP16 and RhoA/phosphatidylinositol 3-kinase (PI3K)/Akt/c-Myc and IKK/IKB/NF-κB signalling pathway-related proteins in NPC cells were measured by qRT-PCR and Western blot (WB). CCK8 assays and colony formation assays were used to detect cell proliferation. Transwell assays were used to detect the migration and invasion ability of NPC cells. Flow cytometry and WB were used to measure the level of apoptosis. For the in vivo study, NPC xenograft models were established in nude mice, and tumour weight and volume were recorded. The expression levels of NOP16 and RhoA/PI3K/Akt/c-Myc signalling pathway-related proteins and mRNAs were measured by immunofluorescence, qRT-PCR and WB experiments. In clinical samples, the results of qRT-PCR and IHC experiments showed that the expression level of NOP16 was significantly increased in NPC tissues. In the in vitro study, the results of qRT-PCR and WB experiments showed that NOP16 was significantly increased in NPC cells. The CCK8 assay, colony formation assay, transwell assay and flow cytometry results showed that knocking out NOP16 inhibited the proliferation, migration and invasion of NPC cells and increased apoptosis. WB results showed that knocking out NOP16 inhibited the RhoA/PI3K/Akt/c-Myc and IKK/IKB/NF-κB signalling pathways. These effects were reversed by 740Y-P (PI3K activator). In the in vivo study, knockdown of NOP16 reduced tumour volume and weight and inhibited the RhoA/PI3K/Akt/c-Myc signalling pathway. In conclusion, knockdown of NOP16 inhibited the proliferation, migration and invasion of NPC cells and induced apoptosis by inhibiting the RhoA/PI3K/Akt/c-Myc and IKK/IKB/NF-κB pathways, leading to the malignant phenotype of NPC.

CircRNA DNA methyltransferase 1 silence inhibits breast cancer development by regulating micoRNA-485-3p/zinc finger E-box binding homeobox 1 axis.

BACKGROUND: Circular RNAs (circRNAs) are associated with tumorigenesis of breast cancer. Nevertheless, how and whether circRNA DNA methyltransferase 1 (circ-DNMT1) controls breast cancer development remains poorly understood. METHODS: The paired tumor and paracancer tissues (n = 41) were obtained from breast cancer patients. Circ-DNMT1, microRNA (miR)-485-3p, and zinc finger E-box binding homeobox 1 (ZEB1) abundances were measured by quantitative reverse transcription polymerase chain reaction and western blot. Cell colony formation, migration, invasion, and apoptosis were analyzed by colony formation analysis, transwell analysis, and flow cytometry. Target relationship was evaluated via dual-luciferase reporter analysis, RNA immunoprecipitation, and pull-down. The in vivo experiments were conducted using a xenograft model. RESULTS: Circ-DNMT1 and ZEB1 levels were upregulated in breast cancer, and miR-485-3p was downregulated. Circ-DNMT1 knockdown restrained cell colony formation, migration, and invasion and increased apoptosis. MiR-485-3p was negatively regulated by circ-DNMT1, and miR-485-3p knockdown mitigated the effect of circ-DNMT1 silence on breast cancer development. ZEB1 was targeted via miR-485-3p, miR-485-3p overexpression repressed cell colony formation, migration, and invasion and triggered apoptosis by decreasing ZEB1. Circ-DNMT1 silence reduced ZEB1 expression via regulating miR-485-3p. Circ-DNMT1 knockdown reduced xenograft tumor growth. CONCLUSION: Circ-DNMT1 knockdown constrains breast cancer development via modulating miR-485-3p/ZEB1 axis.

Origin recognition complex subunit 1 regulates cell growth and metastasis in glioma by altering activation of ERK and JNK signaling pathway.

Origin recognition complex subunit 1(ORC1) is reported to be closely associated with the cell cycle. However, studies on the role of ORC1 in glioma remain undefined. The aim of the present study was to determine whether ORC1 affects cell migration, invasion, apoptosis, and proliferation and to explore the possible underlying mechanism. GEO database analysis indicated that ORC1 was significantly upregulated in glioma, while Gene set enrichment analysis (GSEA) analysis indicated that ORC1 primarily regulated the cell cycle and affects apoptotic signaling pathways. Analysis of protein-protein interaction (PPI) and gene ontology (GO) to further study the relevant mechanisms revealed that the function of the interaction between proteins and ORC1 was primarily concentrated in the regulation of cell cycle, and apoptosis played a critical role in the whole PPI network. Western blot assay and RT-PCR assay indicated that ORC1 was significantly upregulated in glioma tissues. Western blot assay and RT-PCR indicated that ORC1 was significantly upregulated in glioma cell lines. Cell migration, invasion, apoptosis, and proliferation were detected using Transwell and wound healing assays, flow cytometry, colony formation, and CCK8, respectively. Furthermore, OCR1 inhibition reduced invasion and migration, promoted cell apoptosis. In addition, OCR1 overexpression promoted cell proliferation and induced G2 phase arrest. Moreover, OCR1 downregulation suppressed activation of the ERK/JNK signaling pathway. The effects of ORC1 on biological processes were reversed by ERK and JNK inhibitors. These results indicate that ORC1 could be a novel prognostic marker of glioma via the activation of the ERK/JNK signaling pathway.

Intersectin 1 (ITSN1) identified by comprehensive bioinformatic analysis and experimental validation as a key candidate biological target in breast cancer.

BACKGROUND: As one of the most common cancers, breast carcinoma is the most common disease in women. Intersectin 1 (ITSN1) contributes to the actin cytoskeleton reconstruction in breast cancer. PURPOSE: The objective of this study to explore the functions of ITSN1 in breast carcinoma. METHODS: We downloaded microarray datasets GSE8087, GSE50697, and GSE98238 from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were used to construct a protein-protein interaction (PPI) network using STRING database, and the modules from PPI network were verified by Cytoscape software. Gene ontology terms and Kyoto Encyclopedia of Gene and Genome pathway were used to analyze the biological functions using the DAVID database. ONCOMINE, GEPIA, UALCAN, and Human Protein Atlas databases were used to investigate the characteristics of ITSN1 for the prognosis of breast carcinoma. Cell counting kit-8, flow cytometry, and colony formation assays were used to detect cell viability, cell apoptosis, and cell proliferation. RT-PCR and Western blot assays were used to detect ITSN1, Ki67, and cleaved caspase-3 expressions. RESULTS: Low expressions of ITSN1 were significantly associated with clinical cancer stages. RT-PCR and Western blot analysis showed low expression of ITSN1 in breast cancer tissues and cell lines. ITSN1 inhibition could promote cell proliferation and inhibit cell apoptosis, while ITSN1 overexpression could inhibit cell proliferation and increase cell apoptosis by regulating the levels of expression of Ki67 and cleaved-caspase-3. CONCLUSION: The results indicated that ITSN1 could be a prognostic biomarker for survivals of breast cancer patients.

Design of a microfluidic chip consisting of micropillars and its use for the enrichment of nasopharyngeal cancer cells.

The aim of the present study was to discuss the design of a microfluidic chip consisting of columns, and its use for the enrichment of nasopharyngeal cancer (NPC) cells. A microfluidic chip experiment was simulated using FLUENT software. Within the microfluidic chip, aptamers were bound to the reaction chamber (consisting of columns) using a biotin-avidin system. Cell suspension was introduced into the reaction chamber to capture NPC cells. NPC cells were subsequently eluted, and the capture rate of the cells was calculated. The modified aptamer-bound microfluidic chip was able to capture NPC cells with a capture rate of ~90%. The modified aptamer-bound microfluidic chip has a wide range of potential applications for the diagnosis of NPC.