The interleukin-21 (IL-21) protein was found to be expressed at an elevated level in clinical samples of colorectal cancer patients without or with a parasitic infection that were collected from Sudan in our previous study. The IL-21 gene in HT29 and HCT116 cells was then correlated to cell proliferation and cell migration, as well as the cellular mechanisms associated with gene expressions in our present study. Our results demonstrated that silencing the IL-21 gene in HCT116 cells increased the cytotoxic level and fibroblast growth factor-4 (FGF4) mRNA expression in the cancer cells. Moreover, specific gene silencing reduced the migration of cancer cells compared to non-silenced cancer cells. These events were not observed in IL-21-silenced HT29 cells. Neutralizing FGF4 in conditioned medium of IL-21-silenced HCT116 cells further increased the cytotoxic level and restored the migratory activity of HCT116 cells in the culture compared to silencing the IL-21 gene alone in the cancer cells. Our results indicate the importance of both silencing the IL-21 gene and co-expression of the FGF4 protein in HCT116 cells, which pave the way for the discovery of important factors to be used as biomarkers for the design of drugs or cost-effective supplements to effectively treat the patients having infectious disease and HCT116 cells of colorectal cancer simultaneously in the future.

Background: Schistosomiasis is one of the parasitic infections that are often found in humans. More than approximately 200 million people are infected with Schistosomiasis in tropical and subtropical areas of Africa, South America and Asian countries. Literature has long been suggesting the correlation between Schistosomiasis and colorectal malignancy. There is a considerable directory supporting the etiological relation between Schistosoma japonicum infection and colorectal cancer in the Far East, however, the available data about the role of Schistosoma mansoni that can initiate the carcinogenesis of colorectal remain insignificant. Objective: As such, more studies of this disease should be conducted comprehensively for corporate social responsibility internationally. Methods: The present study reviewed the available data about the role of Schistosoma, including S. mansoni in association with the carcinogenesis of colorectal. Results: The study shows the possible evidence of epidemiology, pathology, molecules and immunopathology associated with Schistosomal infections and colorectal cancer. The infections are apparently getting little attention nor support worldwide due to the geographical barriers and some political issues because it mainly occurs in the people living in the bottom billion and happens in the endemic regions only. Conclusion: The in-depth study of this infectious disease will tailor early diagnosis, novel prescription drugs and cost-effective strategies for the treatment of infectious disease colorectal cancer, and hence eradicate the disease in the endemic regions.

Objectives This study aimed to investigate the effects of specific gene silencing in colorectal cancer cells. Clusterin protein was found in the serum samples of colorectal cancer patients infected with Schistosoma mansoni previously. Methods For this reason, silencing clusterin mRNA in colorectal cancer cells was first performed to study the cytotoxic effect by lactate dehydrogenase assay. Next, propidium iodide staining and flow cytometry were performed to investigate the cell cycle profile in clusterin-silenced cells. A wound-healing assay was also used to examine the migration rate of clusterin-silenced cells. The mRNA expression of cell proliferation- and migration-related genes was then assessed by real-time PCR. Results Clusterin mRNA silencing caused a significant reduction in cell growth but induced no cell cycle arrest or potential apoptosis in all cells. It was found in this study that cell migration rate was inhibited in clusterin-silenced cells. Surprisingly, significantly induced chemokine (C–C motif) ligand 5 (CCL5) mRNA expression was detected in clusterin-silenced Caco2, which indicated that the cell proliferation and migration of clusterin-silenced Caco2 were likely associated with CCL5 mRNA expression. Conclusions Clusterin may be a potential target for regulation, staging, surveillance, and developing a cost-effective therapeutic agent for treating parasite-infected Caco2 type of colorectal cancer patients.

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