Survivin Dynamics in Cancer Therapeutics

Survivin, a member of the inhibitor of apoptosis protein family, occupies a central position at the crossroads of cell division and programmed cell death. Highly expressed in most malignancies yet virtually absent from differentiated adult tissues, it contributes to tumour cell survival, resistance to conventional therapies and poor clinical outcome. Mechanistically, survivin modulates mitotic spindle assembly, inhibits caspase activation and engages in complex networks with kinases and chaperones to ensure both proliferation and suppression of apoptosis. Dynamic regulation of survivin involves post-translational modifications such as phosphorylation and ubiquitination that govern its stability and subcellular localisation. Therapeutic strategies have sought to disrupt survivin’s interactions, impede its gene transcription or accelerate its degradation, but clinical translation has been hampered by delivery challenges, compensatory survival pathways and toxicity concerns. Recent advances in small-molecule inhibitors, antisense oligonucleotides, immunotherapy approaches and nanocarrier systems promise more selective targeting. An integrated understanding of survivin’s modulation in distinct cancer contexts is critical for designing combinatorial regimens that can overcome resistance and reinforce tumour cell eradication.

Research from Nature Portfolio

Work on the NF-κB–survivin axis in bladder cancer has revealed that aberrant activation of this inflammatory transcription factor enhances survivin expression, driving cell proliferation and apoptosis evasion. Pharmacological suppression of survivin with a small-molecule inhibitor reinstates apoptotic pathways, diminishes tumour growth in xenograft models and sensitises cells to standard chemotherapeutics. This study underscores the therapeutic promise of targeting upstream regulators of survivin and validates a survivin-centric approach in inflammation-associated malignancies.

Survivin Dynamics in Cancer Therapeutics publication trend

The graph below shows the total number of articles in survivin dynamics in cancer therapeutics across all publications each year (not limited to Nature Index journals).

Technical terms

Survivin: An inhibitor of apoptosis protein that regulates mitosis and suppresses programmed cell death.

NF-κB: A transcription factor that controls genes involved in inflammation, proliferation and cell survival.

Ubiquitination: A post-translational modification tagging proteins for degradation by the proteasome.

Phosphorylation: The covalent attachment of a phosphate group that regulates protein activity and interactions.

Chemoresistance: The capacity of cancer cells to withstand the cytotoxic effects of chemotherapy agents.

Theranostics: Combined diagnostic and therapeutic strategies often using multifunctional delivery systems.

References

1. NF-κB suppresses apoptosis and promotes bladder cancer cell proliferation by upregulating survivin expression in vitro and in vivo. Scientific Reports (2017).
2. Targeting survivin with Tanshinone IIA inhibits tumor growth and overcomes chemoresistance in colorectal cancer. Cell Death Discovery (2023).
3. A Gold Nanocage Probe Targeting Survivin for the Diagnosis of Pancreatic Cancer. Pharmaceutics (2023).
4. Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?. Journal of Experimental & Clinical Cancer Research (2019).