Cancer Genetics and Epigenetics 2024, Vol.12, No.4, 182-193 http://medscipublisher.com/index.php/cge 186 potential to specifically target and degrade E6/E7 mRNAs, further validating these oncogenes as key therapeutic targets in cervical cancer (Chen et al., 2020). 4.2 Host cellular genes Targeting host cellular pathways involved in tumor progression offers another promising avenue for cervical cancer therapy. HPV oncogenes E6 and E7 hijack various cellular mechanisms, including DNA damage repair, cell cycle regulation, and epigenetic modifications, to promote carcinogenesis (Yeo-Teh et al., 2018; Estêvão et al., 2019; Bruyère et al., 2023). For instance, E6 and E7 interfere with the DNA damage response by interacting with and destabilizing key repair proteins, thereby increasing cellular sensitivity to DNA-damaging agents such as radiotherapy (Figure 2). By targeting these host cellular pathways, it is possible to enhance the efficacy of existing treatments and develop new therapeutic strategies (Bruyère et al., 2023). RNAi technology can be employed to silence specific host genes that are critical for tumor cell survival and proliferation, thereby providing a multifaceted approach to combat cervical cancer. Figure 2 Enrichment of DNA Damage/Repair Proteins Targeted by HPV16 E6/E7 in the Nucleoplasmic Fraction and Their Partial Colocalization with E1/E2 (Viral Replication) Foci (Adapted from Bruyère et al., 2023) Image Caption: A: Steps of cycloheximide chase experiment and subcellular protein fractionation; B: Stability and half-life of HPV16 E6/E7 protein targets from HaCaT cells after treatment with cycloheximide; C: Quantification of E6/E7 target proteins
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