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BIRC5

Official Full Name
baculoviral IAP repeat containing 5
Organism
Homo sapiens
GeneID
332
Background
This gene is a member of the inhibitor of apoptosis (IAP) gene family, which encode negative regulatory proteins that prevent apoptotic cell death. IAP family members usually contain multiple baculovirus IAP repeat (BIR) domains, but this gene encodes proteins with only a single BIR domain. The encoded proteins also lack a C-terminus RING finger domain. Gene expression is high during fetal development and in most tumors, yet low in adult tissues. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. [provided by RefSeq, Jun 2011]
Synonyms
API4; EPR-1;
Bio Chemical Class
Acyltransferase
Protein Sequence
MGAPTLPPAWQPFLKDHRISTFKNWPFLEGCACTPERMAEAGFIHCPTENEPDLAQCFFCFKELEGWEPDDDPIEEHKKHSSGCAFLSVKKQFEELTLGEFLKLDRERAKNKIAKETNNKKKEFEETAKKVRRAIEQLAAMD
Open
Disease
Brain cancer, Lung cancer, Multiple myeloma, Solid tumour/cancer
Approved Drug
0
Clinical Trial Drug
4 +
Discontinued Drug
0

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Detailed Information

Crucially part of the inhibitor of apoptosis (IAP) gene family, Birc5, often known as survivin, controls cell death and survival. Unlike other members of this family that usually have several baculovirus IAP repeat (BIR) domains, BIRC5 uniquely generates proteins with a single BIR domain, devoid of the C-terminus RING finger domain. This specific structural characteristic is significant, as it defines BIRC5's functional capabilities within the cell.

The expression of BIRC5 is notably high during fetal development and in various tumor types, while it remains low in adult tissues. This expression pattern indicates a potential role for BIRC5 in cellular growth and proliferation, particularly during critical developmental stages and in pathological conditions like cancer. Studies have identified several alternatively spliced transcript variants of BIRC5, each encoding distinct isoforms that may have differing functional implications.

BIRC5 in Cancer Biology

Birc5 has been linked, according to studies, to various malignancies including adenocarcinoma, cervical intraepithelial neoplasia, lung cancer, colon cancer, pancreatic cancer, prostate cancer, breast cancer, lymphoma, neuroblastoma, and esophageal cancer. Its overexpression in these tumors points to Birc5's likely central importance for cancer cell survival and proliferation. More specifically, the protein stimulates cell proliferation and suppresses death, therefore helping to drive tumor development.

Two main roles may be distinguished from Birc5's many activities: its action as an anti-apoptotic factor and its control of the cell cycle. Birc5 interacts with several proteins in the cytoplasm to block apoptotic pathways, therefore stopping programmed cell death. BIRC5 functions in fundamental processes including DNA repair and transcriptional control in the nucleus, thus affecting cellular responses to damage and stress.

Mechanisms of Action

Well-documented is the protein's capacity to both promote cell growth and prevent death. Crucially important for chromosomal alignment and segregation during mitosis and cytokinesis, Birc5 is a component of the chromosome passage protein complex (CPC). Its significance in preserving genomic integrity is shown by the direction of the CPC to many sites during cell division.

BIRC5 links with histone H3 phosphorylated at 'Thr-3' early in mitosis to help the CPC to be recruited to centromeres. Good chromosomal segregation depends on this interaction. Furthermore, Birc5 forms a scaffold required for the transfer of TPX2, a RAN effector, to microtubules, which is essential for mitotic spindle formation, by interacting with the RAN protein. These connections show how Birc5 combines signaling systems control of cell division.

Additionally proven to offset the normal induction of death usually found in the G2/M phase of the cell cycle is Birc5. Birc5 helps preserve cell viability throughout important periods of cell division by blocking the activation of caspases, especially CASP3 and CASP7. Furthermore underlining BIRC5's regulating function in transcriptional networks, research has shown that the acetylated version of the gene may block STAT3's transactivation of target gene promoters.

Figure 1 describes how the BIRC5 protein functions in the cytoplasm and nucleus, regulating various cellular processes such as cell survival, cell cycle progression, apoptosis inhibition, and mitotic spindle formation.Figure 1. BIRC5 (survivin) functions in the cytoplasm and nucleus, supporting cell survival, cell cycle progression, mitotic spindle formation, and transcription activation. (Rigato, D.B et al., 2020)

Implications for Cancer Therapy

Birc5 is becoming a target for therapeutic intervention as it is quite important in cancer biology. High expression levels of Birc5 in different types of tumors imply that stopping its activity will improve the efficacy of current therapies, including radiation and chemotherapy. For glioblastoma, for instance, focused RNA interference treatments aiming at Birc5 have been demonstrated to lower tumor cell resistance to radiation therapy, therefore slowing down tumor development. In liver and breast cancers as well, medications meant to stop BIRC5 have shown success in slowing tumor growth.

With clinical studies examining Birc5-targeting medications showing encouraging outcomes, the possibility of Birc5 as a therapeutic target has attracted attention recently. This research shows the prospect of creating medicines that especially lower Birc5 levels or inhibit its action, therefore causing death in cancer cells and enhancing the results of therapy.

Regulation of Apoptosis and Autophagy

Particularly in autophagy, emerging studies further suggest that Birc5 could have functions outside of those of control of death. Although Birc5 is not yet proven to be a direct autophagy regulator, certain research has indicated that it may affect this process indirectly. For different cell types, for example, the negative association between Birc5 and ATG7 expression levels suggests that Birc5 could control autophagy-related pathways.

Recent research shows that at a vital stage in the production of autophagosomes, Birc5 interacts with ATG12-ATG5 conjugates. This interaction seems to stop the ATG12-ATG5-ATG16L1 complex from assembling, hence lowering autophagic flux in cancer cells. Fascinatingly, this negative control of autophagy may assist preserve DNA integrity in non-stressed environments, hence complicating the function of Birc5 in cellular homeostasis.

Birc5 is usually missing or expressed extremely low in normal tissues; in many tumors, especially aggressive ones, its expression is much raised. This heterogeneous expression pattern emphasizes the importance of BIRC5 in carcinogenesis and the possible results of its dysregulation.

References:

  1. Lin TY, Chan HH, Chen SH, et al. BIRC5/Survivin is a novel ATG12-ATG5 conjugate interactor and an autophagy-induced DNA damage suppressor in human cancer and mouse embryonic fibroblast cells. Autophagy. 2020;16(7):1296-1313.
  2. Abolfathi H, Arabi M, Sheikhpour M. A literature review of microRNA and gene signaling pathways involved in the apoptosis pathway of lung cancer. Respir Res. 2023 Feb 17;24(1):55.
  3. Rigato, D.B., Branco, P.C., Silva, C., et al. BIRC7 (baculoviral IAP repeat containing 7). Atlas of genetics and cytogenetics in oncology and haematology. 2020.
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