Abstract
The janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway is associated with the regulation of essential cellular mechanisms, such as proliferation, invasion, survival, inflammation, and immunity. Aberrant JAK/STAT signaling contributes to cancer progression and metastatic development. STAT proteins play an essential role in the development of cervical cancer, and the inhibition of the JAK/STAT pathway may be essential for enhancing tumor cell death. Persistent activation of different STATs is present in a variety of cancers, including cervical cancer, and their overactivation may be associated with a poor prognosis and poor overall survival. The oncoproteins E6 and E7 play a critical role in the progression of cervical cancer and may mediate the activation of the JAK/STAT pathway. Inhibition of STAT proteins appears to show promise for establishing new targets in cancer treatment. The present review summarizes the knowledge about the participation of the different components of the JAK/STAT pathway and the participation of the human papillomavirus (HPV) associated with the process of cellular malignancy.
Highlights
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway plays a central role in immune responses, cell proliferation, differentiation, and survival
We focus on the antecedents involving the janus kinase (JAK)/STAT pathway and its relationship with E6/E7 human papillomavirus (HPV) oncoproteins in cervical cancer progression
The JAK/STAT pathway mediates a plethora of regulatory processes of the immune system, including many processes that are involved in tumor cell recognition and tumor-driven immune escape
Summary
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway plays a central role in immune responses, cell proliferation, differentiation, and survival. E7 can regulate epigenetic marks, splice changes, generate regulatory RNAs—regulators of the transcription among other changes that allow the virus to proliferate in an uncontrolled manner—and generate cell transformation and carcinogenesis [7,8,9,10] In this context, multiple publications show how HPV infection increases the activity of proto-oncogenic transcription factors such as those involved in the JAK/STAT pathway. A key feature in the interaction of malignant cells with the tumor microenvironment is their ability to evade or even suppress antitumor immune responses It is well-documented that the differentiation of naïve T cells in various subpopulations depends mainly on the action of cytokines and the signaling pathways that turn on; in this context, the JAK/STAT pathway plays an essential role in the differentiation of CD4 T cells and the action of these on the immunological process. The role of the JAK/STAT pathway in cervical cancer remains poorly understood; it is essential to understand the role of each of the components of the JAK/STAT pathway in the development and control of this neoplasia, which represents a public health problem in developing countries
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