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Survivin (BIRC5): Implications in cancer therapy
Giuseppe Siragusa1, Laura Tomasello1, Carla Giordano1
1Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, Italy.
Abstract:
Inhibitors of Apoptosis proteins (IAPs) were discovered through experiments aimed at rescuing apoptosis in insects. Classically associated with the inhibition of apoptosis, the IAP member Survivin also regulates cell cycle progression and is an essential component of the Chromosomal Passenger Complex (CPC), responsible for chromosomal segregation. Although undetectable in most adult tissues, Survivin is expressed in Adult Stem Cells (ASCs) and plays a crucial role in their maintenance. Survivin is overexpressed in most cancers, contributing to their clonal expansion. As a result, it has been proposed as a possible anticancer target for nearly two decades. In this discussion, we will explore the rationale behind Survivin as a therapeutic target, focusing on common cancer types such as carcinomas, sarcomas, and leukemias. We will delve into the modulation of Survivin by cancer pro-survival cell signaling, the association between SNPs and tumorigenesis, and its regulation by miRNAs. Finally, we will compare cell growth, clonogenic capacity, and apoptosis, along with different strategies for Survivin inhibition, including gene expression and protein activity modulation.
Insights
Survivin, a protein inhibiting apoptosis, is crucial for adult stem cells and cancer progression. Targeting Survivin offers a promising strategy for treating various cancers like carcinomas, sarcomas, and leukemias.
Area of Science:
- * Molecular Biology
- * Cancer Biology
- * Stem Cell Biology
Background:
- * Inhibitors of Apoptosis proteins (IAPs) were initially identified for their role in preventing programmed cell death.
- * Survivin, an IAP member, is vital for cell cycle regulation, chromosomal segregation, and adult stem cell maintenance.
- * Aberrant Survivin expression is common in cancers, promoting tumor growth and survival.
Purpose of the Study:
- * To explore the rationale for targeting Survivin as an anticancer therapeutic.
- * To examine Survivin's role in various cancer types, including carcinomas, sarcomas, and leukemias.
- * To review Survivin's regulation by cancer signaling pathways, genetic variations (SNPs), and microRNAs (miRNAs).
Main Methods:
- * Review of existing literature on Survivin's function and therapeutic targeting.
- * Analysis of Survivin's involvement in cancer pro-survival signaling.
- * Examination of the relationship between Survivin single nucleotide polymorphisms (SNPs) and tumorigenesis.
- * Investigation of Survivin regulation by miRNAs.
- * Comparison of cell growth, clonogenic potential, and apoptosis under different inhibition strategies.
Main Results:
- * Survivin overexpression is linked to enhanced cell proliferation, survival, and resistance to apoptosis in cancer cells.
- * Survivin's role in adult stem cell maintenance suggests potential on-target toxicities with therapeutic inhibition.
- * Genetic variations (SNPs) in the Survivin gene may influence cancer risk and progression.
- * miRNAs play a significant role in regulating Survivin expression and function.
- * Various strategies, including gene expression and protein activity modulation, are being explored for Survivin inhibition.
Conclusions:
- * Survivin is a validated therapeutic target due to its critical role in cancer cell survival and proliferation.
- * Understanding Survivin's complex regulation by signaling pathways, genetics, and miRNAs is essential for effective therapeutic development.
- * Diverse approaches to inhibit Survivin, targeting gene expression or protein activity, hold promise for cancer treatment.
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