Cervical cancer (CC) is a serious global health issue, and it is well-known that HPV infection is the main etiological factor that triggers carcinogenesis. In cancer, chemokine ligands and receptors are involved in tumor cell growth, metastasis, leukocyte infiltration, and angiogenesis; however, information on the role played by E6/E7 of HPV16/18 in the modulation of chemokines is very limited. Therefore, this study aimed to determine whether chemokines are differentially expressed in CC-derived cell lines; if E6/E7 oncoproteins from HPV16 and 18 are capable of mediating chemokine expression, what is the expression profile of chemokines in tissues derived from CC and what is their impact on the overall survival of patients with this pathology? For this purpose, RNA sequencing and real-time PCR were performed on SiHa, HeLa, and C33A tumorigenic cell lines, on the non-tumorigenic HaCaT cells, and the E6/E7 HPV-transduced HaCaT cell models. Furthermore, chemokine expression and survival analysis were executed on 304 CC and 22 normal tissue samples from The Cancer Genome Atlas (TCGA) repository. The results demonstrate that CXCL1, CXCL2, CXCL3, and CXCL8 are regulated by E6/E7 of HPV16 and 18, are overexpressed in CC biopsies, and that their higher expression is related to a worse prognostic survival.

The molecular and cell biology of cervical cancer will be covered in detail in this chapter, particularly emphasizing the diseases etiology, brief epidemiology, risk factors, cervical cancer hallmarks, and the main signaling pathways involved. The chapter will go in-depth about the characteristics of cancer, such as changes in cell cycle regulation, apoptosis, and cell differentiation, as well as the tumoral microenvironment. Signal pathways like the PI3K/AKT/mTOR pathway and the Wnt/beta-catenin pathway will be highlighted for their significance in the development of cervical cancer. The chapter will thoroughly explain the molecular and cell biology underlying this terrible illness.