The Role of Chemokines in Cervical Cancers

Abstract

Both clinical-pathological and experimental studies have shown that chemokines play a key role in activating the immune checkpoint modulator in cervical cancer progression and are associated with prognosis in tumor cell proliferation, invasion, angiogenesis, chemoresistance, and immunosuppression. Therefore, a clear understanding of chemokines and immune checkpoint modulators is essential for the treatment of this disease. This review discusses the origins and categories of chemokines and the mechanisms that are responsible for activating immune checkpoints in cervical dysplasia and cancer, chemokines as biomarkers, and therapy development that targets immune checkpoints in cervical cancer research.

The Value of CXCL1, CXCL2, CXCL3, and CXCL8 as Potential Prognosis Markers in Cervical Cancer: Evidence of E6/E7 from HPV16 and 18 in Chemokines Regulation

“…Furthermore, they control immune cell biology characteristics such as activation, recruitment, phenotype, and function by controlling their location and interactions in lymphoid tissues and the TME [52,53]. The role of chemokines is complex, as their expression is regulated by immune cells, stromal cells, and tumor cells, contributing to both anti-and pro-tumorigenic immune responses, relying on various factors [54].…”

The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics

“…[24] Previous studies also confirmed that suppression of CXCL2 in cervical cancer cells could significantly inhibited clonogenic growth and cell proliferation. [25] VEGFa therapy has been well used in the treatment of cervical cancer, [26,27] and studies have confirmed that VEGFa may activate PI3K/Akt and its downstream mTOR signaling pathway and promote the growth and invasion of cervical cancer cells. [28] HK2 is a member of the HK family and is an enzyme that catalyzes the conversion of glucose to glucose-6-phosphate.…”

Expression profiling of mRNA and functional network analyses of genes regulated by human papilloma virus E6 and E7 proteins in HaCaT cells

“…This partly explains the almost undetectable activation of potent anti-tumor immune responses in primary HPV-infected epithelial tissues. It has been reported that humans lack a robust inflammatory response against primary HPV infection and progressively lose immune cells in the cervical stroma during CIN ( Kleine-Lowinski et al, 2003 ; Hacke et al, 2010 ; Garrido et al, 2021 ). CIN is strongly associated with CCL2 expression in the tumor microenvironment.…”