The role of Nuclear Factor-kappa B signaling in human cervical cancer.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms without systematic review methodology or new clinical data.
PubMed 29198328 · doi:10.1016/j.critrevonc.2017.11.001
What was done
The authors conducted a narrative review summarizing the biological mechanisms and signaling networks of Nuclear Factor-kappa B (NF-kB) in the initiation, progression, and treatment resistance of human cervical cancer, including its crosstalk with HPV and other oncogenic pathways.
What was found
The abstract reports no numerical findings or effect estimates. It outlines that HPV initial infection leads to downregulation of NF-kB to evade immune-mediated replication inhibition, allowing persistent infection. During progression to high-grade intraepithelial neoplasia and invasive cancer, NF-kB becomes constitutively activated. Downstream effects include the upregulation of proliferative genes (such as cyclin D1 and c-myc), VEGF-driven angiogenesis, telomerase activation, and induction of mutagenic APOBEC and AID enzymes.
Why it matters
This review integrates mechanistic pathways linking HPV persistence and NF-kB activation to cervical cancer progression, illustrating how NF-kB pathway inhibition could theoretically help overcome resistance to radiotherapy and chemotherapy.
Limits
The abstract describes a narrative review with no systematic search methodology, meta-analysis, or primary clinical data. The review notes that clinically active direct NF-kB targeting strategies are not yet available for treatment.
Cited by
- supports The transcription factor NF-κB regulates about 200 genes involved in immune response and regulates vascular endothelial growth factor (VEGF).