The purpose of this chapter is to explore student activism within community colleges, including opportunities for and barriers to activism. The authors argue that community colleges can and should leverage curricular and co-curricular venues to teach about and promote activism, thus encouraging socio-academic integrative moments that combine both academic and social integration. While four-year institutions might engage students in learning about and practicing activism via opportunities primarily outside of the classroom such as student affairs offices and student leadership opportunities, community colleges can encourage greater student activism primarily in curricular contexts. Indeed, given the demographic diversity present in community colleges—where students often work part- or full-time off campus, spend little time on campus outside of coursework, and have significant personal and family responsibilities—the classroom may be the optimal venue to engage students.
The purpose of this chapter is to explore student activism within community colleges, including opportunities for and barriers to activism. The authors argue that community colleges can and should leverage curricular and co-curricular venues to teach about and promote activism, thus encouraging socio-academic integrative moments that combine both academic and social integration. While four-year institutions might engage students in learning about and practicing activism via opportunities primarily outside of the classroom such as student affairs offices and student leadership opportunities, community colleges can encourage greater student activism primarily in curricular contexts. Indeed, given the demographic diversity present in community colleges—where students often work part- or full-time off campus, spend little time on campus outside of coursework, and have significant personal and family responsibilities—the classroom may be the optimal venue to engage students.
Increased levels of reactive oxygen/nitrogen species are one hallmark of chronic inflammation contributing to the activation of pro-inflammatory/proliferative pathways. In the cancers analyzed, the tetrahydrobiopterin:dihydrobiopterin ratio is lower than that of the corresponding normal tissue, leading to an uncoupled nitric oxide synthase activity and increased generation of reactive oxygen/nitrogen species. Previously, we demonstrated that prophylactic treatment with sepiapterin, a salvage pathway precursor of tetrahydrobiopterin, prevents dextran sodium sulfate–induced colitis in mice and associated azoxymethane-induced colorectal cancer. Herein, we report that increasing the tetrahydrobiopterin:dihydrobiopterin ratio and recoupling nitric oxide synthase with sepiapterin in the colon cancer cell lines, HCT116 and HT29, inhibit their proliferation and enhance cell death, in part, by Akt/GSK-3β–mediated downregulation of β-catenin. Therapeutic oral gavage with sepiapterin of mice bearing azoxymethane/dextran sodium sulfate–induced colorectal cancer decreased metabolic uptake of [18F]-fluorodeoxyglucose and enhanced apoptosis nine-fold in these tumors. Immunohistochemical analysis of both mouse and human tissues indicated downregulated expression of key enzymes in tetrahydrobiopterin biosynthesis in the colorectal cancer tumors. Human stage 1 colon tumors exhibited a significant decrease in the expression of quinoid dihydropteridine reductase, a key enzyme involved in recycling tetrahydrobiopterin suggesting a potential mechanism for the reduced tetrahydrobiopterin:dihydrobiopterin ratio in these tumors. In summary, sepiapterin treatment of colorectal cancer cells increases the tetrahydrobiopterin:dihydrobiopterin ratio, recouples nitric oxide synthase, and reduces tumor growth. We conclude that nitric oxide synthase coupling may provide a useful therapeutic target for treating patients with colorectal cancer.
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