CDC25C Antibodies

M-phase inducer phosphatase 3 (CDC25C)

Functions as a dosage-dependent inducer in mitotic control. Tyrosine protein phosphatase required for progression of the cell cycle.

When phosphorylated, highly effective in activating G2 cells to prophase. Directly dephosphorylates CDK1 and activates its kinase activity.

Gene Information

Human
Gene Name:	CDC25C
Uniprot:	P30307
Entrez:	995

Family

Belongs to:
MPI phosphatase family

Alternative Names

CDC 25; CDC25; CDC25C; cell division cycle 25 homolog C (S. cerevisiae); cell division cycle 25 homolog C (S. pombe); cell division cycle 25C; Dual specificity phosphatase Cdc25C; EC 3.1.3.48; mitosis inducer CDC25; M-phase inducer phosphatase 3; phosphotyrosine phosphatase

Molecular Weight

Mass (kDA):
53.365 kDA

Genomic Context

Human
Location:	5q31.2
Sequence:	5; NC_000005.10 (138285265..138338355, complement)

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Malignant Neoplasm Of Prostate
• Cell Transformation, Neoplastic
• Malignant Tumor Of Colon
• Leukemia
• Prostatic Neoplasms
• Malignant Neoplasm Of Lung
• Lung Neoplasms
• Liver Carcinoma

• Ataxia
• Colonic Neoplasms
• Ataxia Telangiectasia
• Malignant Squamous Cell Neoplasm
• Malignant Paraganglionic Neoplasm
• Neoplasm Metastasis
• Liver Neoplasms

Interacting Proteins

• CDK1
• CHEK1
• LZTS1
• PLK1
• YWHAB

Pathways

• Cell Cycle
• Cell Cycle Arrest
• Mitosis
• Cell Growth
• Cell Proliferation
• Cell Death
• Cell Division
• S Phase
• Localization
• M Phase
• Induction Of Apoptosis
• Dna Damage Checkpoint
• Cell Cycle Checkpoint

• G2 Phase
• Interphase
• Dna Replication
• Dna Repair
• Hyperphosphorylation
• Meiosis
• Metaphase

PTMs

• Phosphorylation
• Dephosphorylation
• Cleavage
• Ubiquitination
• Methylation
• Reduction
• Acetylation
• Demethylation

• Sumoylation
• Phosphorothioation
• Glutathionylation
• Amidation
• Citrullination
• Ribosylation
• Biotinylation
• Deacetylation

• Oxidation

Research Areas

• Cell Cycle and Replication
• Phospho-Specific
• Protein Phosphatase

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CDC25C

Best Uses Of The CDC25C Marker

Many applications can be made of the CDC25C marker. It regulates the G2/M cell cycle and is involved in DNA damage repairs. This marker is a potent early tool for hepatocellular carcinoma detection. CDC25B antibodies are made by Boster Bio. This article offers more details about the CDC25C marker. We'll discuss the ways this protein can be used to detect hepatocellular cancer.

The CDC25C tumor marker is

CDC25C is a key cell cycle regulator and may play an important role in cancer treatment. This tumor-associated antigen can be found in many types of cancer including female Squamous cell carcinoma. Therefore, identifying a tumor that has high levels of CDC25C may provide new insights into cancer treatment. In addition to helping in the diagnosis of cancer, CDC25C can also help in the early detection of malignancies.

The tumors expressing high levels of CDC25C can be considered advanced. High levels of CDC25C suggest an advanced FIGO stage and lymph node metastasis and the size of the tumor and degree of differentiation. Overexpression of CDC25C is associated with a greater rate and longer survival. However it is necessary to conduct more research to determine if the CDC25C gene is an actual cancer marker or an effective biomarker.

The CDC25C protein is a member of the specific phosphatase phosphatase group. It is involved in the transformation of mitotic cells into G2/M and regulates the cyclin B1/CDK1 component. It is involved in the regulation of checkpoint proteins which ensures accurate DNA information is transferred to daughter cells. In addition, it could be a potential new therapy for cancer, as overexpression may be linked to activation of the CDK1/cyclin B1 complex.

The most common type of cancer in which the CDC25C protein is overexpressed is prostate cancer. The protein is expressed in various forms and is also elevated in prostate tumors. Overexpression of CDC25A has also been associated with a lower prognosis. Although CDC25A is not a cause of tumor development, it may play a role in RAS transformation as an orcogene that limits the rate of growth. Furthermore, CDC25C point mutations are a critical part of acute myelogenemia.

CDC25C is a differentially expressed protein in the cell's cytoplasm. CDC25C moves from the cytoplasm into the nucleus during interphase. In turn, its location is controlled by the rate of import and export. The CDC25C NES sequence controls movement from the cytoplasm to the nucleus. The enzyme PLK1 activates the Ser191 and Ser198 residues of CDC25C which aids in nuclear translocation.

G2/M progression is controlled by CDC25C

The G2/M checkpoint is controlled through the CDC25A/CDC25C family of proteins. In the presence of the inhibitor of topoisomerase II etoposide cells in G2 are able to complete mitosis only when they lack Cdc25A. This is a new finding, as Cdc25A was known to regulate G1/S progression. Its stability isn't completely known.

CDC25C, a new MAPK-related target, interacts directly with ERK1/2's Ser216 residue. This interaction promotes activation of CDC25C in the G2/M transition and also promotes its ubiquitination and degradation. In addition an ongoing G2 phase halt requires proteolysis of CDC25C. Translocation of nuclear material is made possible by the phosphorylation process of Ser191 or Ser198 within CDC25C.

PLK1 phosphorylates the CDC25C NES which results in nuclear translocation. Nuclear translocation of the cyclin-B1/CDK1 complex is stimulated by CDC25C. The nuclear translocation of CDC25C is associated with the activation of PLK1. PLK1 negatively regulates the CDC25C Kinase.

CDC25C is a novel partner in the regulation and down-regulation of P53 transcription. It has a DNA binding site and causes G2/M arrest after DNA damage. In addition, CDC25C's promoter inhibits P53 via a p53 reaction element. CDC25C is closely associated with P53 and is controlled by synergists.

In addition to its function in regulating the progression of G2/M CDC25A promotes S-phase, which is the final phase of the cell cycle. It regulates the activity and metabolism of the cyclin B–Cdk1 complex which is essential for mitosis. It can even delay the cell division process. If Cdc25A levels are low, it could interfere with the cyclin B/Cdk1 protein and delay mitosis.

Another function of CDC25C involves the regulation of the cell cycle's advancement. It is closely linked to the growth of tumors and to the development of tumors. The process of tumorigenesis is connected to hyperphosphorylation Cdc25C Ser216. This makes CDC25C an important target for newer cancer treatments. Once fully understood, the CDC25 family will become a vital player in the fight against cancer.

CDC25C mediates DNA damage repair

CDC25C mediates DNA damage repair by controlling the expression of the survivin and Cdc2 genes. After doxorubicin treatment both survivin mRNAs and CDC25C were reduced, but they were rescued by the addition of Zebularine. The doxorubicin and zebularine treatments showed similar protein expressionlevels, however, there no significant changes in the expression of mRNA. The genes weren't expressed in a manner that was in correlation with protein turnover. This suggests that they play separate roles in the repair and preservation of DNA damage.

There is a great deal of evidence to support that CDC25C is a regulator of many important genes that are involved in the progression of the cell cycle. There are contradicting reports regarding the role of CDC25C regulators PLK1 (p53) and p53 (p53). Although CDC25C has multiple functions in DNA repair, there are many distinct theories regarding its control. Contrary to this, p53 plays a direct regulatory role in the regulation of genes whose expression is necessary for the cell cycle.

CDC25C plays a crucial role in cell cycle progression and mitosis, in addition its function as a DNA damage repair agent. Recent research has shown that CDC25C plays a role in cell arrest following DNA damage by activating Cdc25C and phosphorylating CDC1/CDC2. In this instance SB-218078 blocks CDC25C-induced dephosphorylation and microinjection of purified CDC25C protein shifted cells into mitosis. Additionally, zebularine helps to reduce p53-mediated repression of endogenous Cdc25C and Cdc2.

The CDC25C gene promor contains elements that play a role in p53 dependent transcriptional downregulation. This component appears to be functional at background levels in genome-wide ChIP studies. It is not clear whether CDC25C's p53 dependent transcriptional repression relies on p53. CDC25C is also devoid of p21 binding and this is in line with its low copy-number and lack of functional activity.

The repression of Cdc25C gene was validated by a zebularine-doxorubicin experiment in HCT116 cells. It is interesting to note that zebularine entrapment caused the re-expression Cdc25C gene. These findings provide a new method of understanding how Cdc25C gene regulates DNA damage. It is also possible that Cdc25C is involved in repression of genes.

CDC25C is an instrument for diagnosis that can be used in the diagnosis of the early stages of hepatocellular carcinoma.

CBioPortal database was used to study the tissues of HCC patients for CDC25C gene mutations. Mutations in CDC25C were identified in 14 tumor samples from the TCGA-HCC database. These mutations could aid in the clinical diagnosis and monitoring of HCC patients. This study also investigated the interaction between CDC25C with other genes. The results were summarized in Figure 5.

The expression of this gene was significantly elevated in HCC patients from stage 1 to stage 4 and was correlated with overall survival. CDC25C expression was also correlated with patient's gender, grade and race. Stage 1 was the one with the highest levels of CDC25C. However, expression levels dropped significantly in stage 4.

A recent study by Al-Matouq and co. discovered that the CDC25C gene was found to be elevated in a majority of cases of skin cancer. Furthermore, elevated CDC25B and CDC25C levels were detected in blood samples of patients with hepatocellular carcinoma. Although the findings of the research are still in the beginning, they could ultimately aid in developing new treatments for HCC patients.

Combining CDC25C with AFP immunohistochemistry could help detect hepatocellular cancer earlier. HCC is the second-leading cause of cancer-related deaths in the world, and chronic hepatitis is one of the major risk factors. HCC is also more common in people suffering from non-alcoholic steatohepatitis and diabetes. The screening for HCC is vital to the overall survival of a patient and is especially important for those suffering from advanced cirrhosis.