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Gastric cancer (GC) is one of the leading causes of tumor-related mortality. In addition to surgery and endoscopic resection, systemic therapy remains the main treatment option for GC, especially for advanced-stage disease and for cases not suitable for surgical therapy. Hence, improving the efficacy of systemic therapy is still an urgent problem to overcome. In the past decade, the essential roles of microRNAs (miRNAs) in tumor treatment have been increasingly recognized. In particular, miRNAs were recently shown to reverse the resistance to chemotherapy drugs such as 5-fluorouracil, cisplatin, and doxorubicin. Synthesized nanoparticles loaded with mimics or inhibitors of miRNAs can directly target tumor cells to suppress their growth. Moreover, exosomes may serve as promising safe carriers for mimics or inhibitors of miRNAs to treat GC. Some miRNAs have also been shown to play roles in the mechanism of action of other anti-tumor drugs. Therefore, in this review, we highlight the research progress on microRNA-based therapy in GC and discuss the challenges and prospects associated with this strategy. We believe that microRNA-based therapy has the potential to offer a clinical benefit to GC patients, and this review would contribute to and motivate further research to promote this field toward this ultimate goal.

Background: Dicerandrol B is a natural antitumor agent that can be isolated from the endophytic fungus, Phomopsis sp. The present study investigated the effects of dicerandrol B on human cervical cancer HeLa cells. Materials and methods: In this study, dicerandrol B was identified by electrospray ionization mass spectrometry and nuclear magnetic resonance spectroscopy. We used MTT to detect the cell viability. Flow cytometry was used to analyze the apoptosis and cell cycle. Western blot was used to examine the expression of related proteins. Results: Dicerandrol B was isolated from the endophytic fungus Phomopsis sp. The MTT assay and flow cytometry showed that dicerandrol B significantly inhibited HeLa cell viability and induced G2/M cell cycle arrest. Western blot analysis demonstrated that dicerandrol B increased the levels of GRP78, ubiquitin, cleaved PARP, and Bax protein, decreased the levels of PARP and Bcl-2 protein, and caused an increase in the Bax/Bcl-2 ratio in HeLa cells. Dicerandrol B increased the production of ROS in HeLa cells, which was attenuated by the antioxidant N-acetyl-l-cysteine. Conclusion: These findings suggest that dicerandrol B induces apoptosis in human HeLa cells, possibly through the endoplasmic reticulum stress and mitochondrial apoptotic pathways. This suggests that dicerandrol B possesses strong anticancer activity in cervical cancer and provides insight into the underlying mechanisms.

Integrated studies of accumulated data can be performed to obtain more reliable information and more feasible measures for investigating potential diagnostic biomarkers of gastric cancer ( GC ) and to explore related molecular mechanisms. This study aimed to identify micro RNA s involved in GC by integrating data from The Cancer Genome Atlas ( TCGA ) and Gene Expression Omnibus. Through our analysis, we identified hsa‐miR‐17 (miR‐17) as a suitable candidate. We performed a meta‐analysis of published studies and analyzed clinical data from TCGA to evaluate the clinical significance and diagnostic value of miR‐17 in GC . miR‐17 was found to be upregulated in GC tissues and exhibited a favorable value in diagnosing GC . In addition, we predicted that 288 target genes of miR‐17 participate in GC ‐related pathways. Enrichment of Kyoto Encyclopedia of Genes and Genomes pathway, Gene Ontology analysis, and protein–protein interaction analysis of the 288 target genes of miR‐17 were also performed. Through this study, we identified possible core pathways and genes that may play an important role in GC . The possible core pathways include the cAMP , phosphoinositide‐3‐kinase–Akt, Rap1, and mitogen‐activated protein kinase signaling pathways. miR‐17 may be involved in several biological processes, including DNA template transcription, the regulation of transcription from RNA polymerase II promoters, and cell adhesion. In addition, cellular components (such as cytoplasm and plasma membrane) and molecular functions (such as protein binding and metal ion binding) also seemed to be regulated by miR‐17.