Cancer remains one of the most frequently diagnosed diseases worldwide. Among its various forms, colorectal cancer (CRC) consistently ranks among the leading causes of cancer-related morbidity and mortality. CRC is a malignant tumor that arises in the...
Cancer remains one of the most frequently diagnosed diseases worldwide. Among its various forms, colorectal cancer (CRC) consistently ranks among the leading causes of cancer-related morbidity and mortality. CRC is a malignant tumor that arises in the colon or rectum, primarily driven by genetic predisposition and dietary changes. A range of therapeutic strategies—such as surgical resection, radiotherapy, and chemotherapy—has been developed and implemented to combat CRC. However, despite technological and clinical advancements, the prognosis for patients with metastatic CRC remains poor. Surgical resection is particularly limited, as it is not applicable to individuals with advanced-stage disease. Radiotherapy and chemotherapy also damage normal tissues, and tumors often develop resistance to both radiation and anticancer drugs. Consequently, identifying novel therapeutic candidates for patients with advanced CRC is urgently needed.
Natural compounds have long been explored as pharmacologically active agents for a wide range of diseases, including cancer. Flavonoids constitute one of the most prevalent classes of bioactive molecules in nature and have been extensively investigated for their anticancer potential across various cancer types. Naringenin, a flavonoid, and genistein, an isoflavone, have both been studied for their anticancer activities in multiple cancer cell models. However, the precise molecular mechanisms underlying their effects in colorectal cancer cells remain incompletely understood. Therefore, the aim of this study was to evaluate the anticancer effects of naringenin and genistein in colorectal cancer cells and to elucidate the apoptotic pathways involved. In this work, human colorectal cancer HCT-15 cells were utilized.
The methodology of this study was structured into three major components: an anti-proliferation analysis, an apoptosis investigation, and a mechanistic exploration. In the anti-proliferation experiments, cell viability and colony-formation assays demonstrated that increasing concentrations of naringenin and genistein progressively suppressed the growth of HCT-15 cells. Wound healing assays further revealed a marked reduction in cell motility following treatment with either compound. In the apoptosis assessment, comet assays confirmed that naringenin and genistein induced apoptotic cell death and DNA fragmentation, as visualized through fluorescence microscopy. Finally, in the mechanistic analysis, Western blotting showed that treatment with naringenin and genistein upregulated pro-apoptotic proteins while downregulating anti-apoptotic proteins. These results indicate that both compounds activate apoptotic pathways and disrupt survival signaling in HCT-15 cells. Collectively, these findings suggest that naringenin and genistein possess strong therapeutic potential against CRC, provide meaningful mechanistic insights into their anticancer activity, and support their continued development as effective therapeutic candidates.