
Uncovering NF-κB Dysregulation in Kidney Cancer Subtypes
🧠 Introduction
Renal cell carcinoma (RCC), the most common form of kidney cancer, remains a major clinical challenge due to its complex genetic makeup and elusive molecular drivers. A new review sheds light on how the nuclear factor kappa B (NF-κB) pathway—an essential regulator of inflammation and cell survival—is dysregulated across different RCC subtypes, fueling tumor development and resistance to therapy.
🔍 Research Summary
The review examines the intricate mechanisms of NF-κB dysregulation in clear cell RCC (ccRCC), papillary RCC (PRCC), and chromophobe RCC (chRCC). Normally, the NF-κB pathway acts as a cellular safeguard, regulating responses to immune threats and DNA damage. However, in RCC, multiple layers of this pathway—including upstream receptors like TLR2, transcription factors like RelA, and downstream targets such as HIF-1α—become persistently activated.
This constitutive activity promotes a tumor-friendly environment by enhancing cell proliferation, survival, angiogenesis, and migration. The authors also highlight how this dysregulation interacts with other critical pathways such as PI3K/Akt, further amplifying RCC pathogenesis. Using both in silico analyses of RCC patient data and existing molecular studies, the review presents a comprehensive map of the disrupted NF-κB landscape in kidney cancer.
🌍 Broader Impact
As part of APMAD’s mission to advance precision medicine in oncology, this research provides important insight into the molecular underpinnings of RCC. Targeting the NF-κB pathway—and its dysregulated components—may offer new therapeutic opportunities, particularly for patients with aggressive or treatment-resistant forms of kidney cancer.
📎 Reference
@article{Jayab2025, title = {The molecular mechanism of NF-κB dysregulation across different subtypes of renal cell carcinoma}, journal = {Journal of Advanced Research}, volume = {72}, pages = {501--514}, year = {2025}, issn = {2090-1232}, doi = {https://doi.org/10.1016/j.jare.2024.07.030}, author = {Nour Abu Jayab and Alaa Abed and Iman M. Talaat and Rifat Hamoudi} }
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