Background: A great challenge of cancer chemotherapy is to eliminate cancer cells and concurrently maintain the quality of life (QOL) for cancer patients. Previously, we identified a novel anti-cancer bioactive peptide (ACBP), a peptide induced in goat spleen or liver following immunization with human gastric cancer protein extract. ACBP alone exhibited anti-tumor activity without measurable side effects. Thus, we hypothesize that ACBP and combined chemotherapy could improve the efficacy of treatment and lead to a better QOL.

MicroRNAs (miRNAs or miRs) is a non-coding small RNA of a type of 18~24 nucleotide-regulated gene that has been discovered in recent years. It mainly degrades the target gene mRNA or inhibits its translation process through the complete or incomplete bindings with 3'UTR of target genes, followed by the regulation of individual development, apoptosis, proliferation, differentiation and other life activities through the post-transcriptional regulation. Among many miRNAs, the microRNA family, miR-30, plays diverse roles in these key process of neoplastic transformation, metastasis, and clinical outcomes in different cancer progression. As key member of miR-30, miR-30c is regulated by oncogenic transcription factors and cancer progression related genes. Recently, numerous studies have demonstrated that the aberrant expression of miR-30c was significantly associated with the majority of human cancer progression. In this review, the diverse roles of miR-30c in different cancer progression such as the cellular and molecular mechanisms, the potential applications in clinics were summarized to speculate the benefits of miR-30c over-expression in cancer treatment and prognosis.

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The interplay between tumor cells and mesenchymal stem cells (MSCs) within tumor microenvironment plays a significant role in tumor development, and thus might be exploited for therapeutic intervention. In this study, we isolated MSCs from normal gingival tissue (GMSCs), and detected the effect of GMSCs on oral cancer cells via direct co-culture and indirect co-culture systems. The cell proliferation assay of direct co-culture showed that GMSCs could inhibit the growth of oral cancer cells. Conditioned medium derived from GMSCs (GMSCs-CM) also exerted an anticancer effect, which indicates that soluble factors in GMSCs-CM played a dominant role in GMSCs-induced cancer cell growth inhibition. To investigate the mechanism, we performed apoptosis assay by flow cytometry, and confirmed that cancer cell apoptosis induced by GMSCs could be a reason for the effect of GMSCs on the growth of oral cancer cells. Western blotting also confirmed that GMSCs could upregulate expression of pro-apoptotic genes including p-JNK, cleaved PARP, cleaved caspase-3, Bax expression and downregulate proliferation- and anti-apoptosis-related gene expression such as p-ERK1/2, Bcl-2, CDK4, cyclin D1, PCNA and survivin. Importantly, the inhibitory effect of GMSCs on cancer cells can partially be restored by blockade of JNK pathway. Moreover, animal studies showed that GMSCs exerted an anticancer effect after oral cancer cells and GMSCs were co-injected with oral cancer cells. Taken together, our data suggest that GMSCs can suppress oral cancer cell growth in vitro and in vivo via altering the surrounding microenvironment of oral cancer cells, which indicates that GMSCs have a potential use in the management of oral dysplasia and oral cancer in future.

MicroRNAs are short, single-stranded non-coding RNA molecules that function as regulators of tumor progression in various cancers, including glioma. The present study sought to investigate the biological functions of miR-9-3p in glioma progression. The results of a microRNA microarray indicated that microRNA-9-3p (miR-9-3p, miR-9*) is down-regulated in high-grade (grades III and IV) gliomas compared with non-tumor tissues. These results were confirmed with real-time PCR. The miR-9-3p expression level was associated with age and tumor grade. Herpud1 was regulated by miR-9-3p in glioma cells and tissues and was identified as a miR-9-3p target with luciferase reporter assays. Glioma cells transfected with miR-9-3p mimics or HERPUD1-RNAi had more apoptotic cells than them in control after induced by H2O2. Our results indicated that low expression of miR-9-3p results in a high level of Herpud1, which may protect against apoptosis in glioma.