SPINK1 Antibodies

Serine protease inhibitor Kazal-type 1 (SPINK1)

Serine protease inhibitor which shows anti-trypsin activity (PubMed:7142173). In the pancreas, protects against trypsin-catalyzed premature activation of zymogens (By similarity).

.

Gene Information

Human
Gene Name:	SPINK1
Uniprot:	P00995
Entrez:	6690

Family

Belongs to:
No superfamily

Alternative Names

pancreatic secretory trypsin inhibitor; PCTT; PCTTSpink3; PSTI; PSTISerine protease inhibitor Kazal-type 1; serine peptidase inhibitor, Kazal type 1; serine protease inhibitor, Kazal type 1; SPINK1; Spink3; TATI; TATITumor-associated trypsin inhibitor

Molecular Weight

Mass (kDA):
8.507 kDA

Genomic Context

Human
Location:	5q32
Sequence:	5; NC_000005.10 (147824580..147839231, complement)

Subcellular Localizations

Secreted.

Diseases

• Pancreatitis
• Pancreatitis, Chronic
• Fibrosis
• Malignant Neoplasms
• Cystic Fibrosis
• Acute Pancreatitis
• Malignant Neoplasm Of Pancreas
• Diabetes Mellitus
• Pancreatitis, Alcoholic
• Pancreatic Neoplasm
• Pain

• Acute Recurrent Pancreatitis
• Neoplasms
• Pancreatic Diseases
• Malignant Neoplasm Of Prostate
• Inflammation

Pathways

• Secretion
• Pathogenesis
• Trypsinogen Activation
• Autophagy
• Inflammatory Response
• Cell Proliferation
• Localization
• Cell Death
• Transport
• Protein Secretion
• Hormone Secretion
• Regeneration
• Autophagic Cell Death

• Cell Growth
• Protein Phosphorylation
• Cell Adhesion
• Cell Migration
• Proteolysis
• Immune Response
• Reflex

PTMs

• Phosphorylation
• Methylation

• Cleavage
• Glycosylation

Research Areas

• Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SPINK1

Best Uses of the SPINK1 Marker

SPINK1 has many applications in the field of cancer research. SPINK1 plays a role in the regulation and maintenance of EGFR. Therefore, any therapeutic intervention that is rational should focus on the interaction between SPINK1 and EGFR. But what are the most effective uses for SPINK1? These will be discussed in this article. They will be discussed in conjunction with Neutralization and ELISA.

ELISA assay

The Boster Bio SPINK1 ELSA assay is validated to detect SPINK1 in tumor cells. This enzyme-linked immunosorbent assay (ELISA) is a fast non-invasive method to measure SPINK1 levels in tumor cells. This test is compatible with a range of tumor types and can be used in both mouse and human models.

The test is highly sensitive and specific , and is particularly useful for detect ovarian cancer cells which have metastasized from their primary tumor. The SPINK1 protein can inhibit the development of metastatic lesions in the omentum as well as the peritoneum where tumor cells are generally found. To survive in this environment, cancer cells must be able to resist against anoikis. This is a process normally triggered by loss in cell-matrix interactions. This is only possible if cancer cells can survive in the ascites fluid in a cluster. The SPINK1 protein induces cell death under anchorage-independent conditions.

The SPINK1 ELISA test can be used to measure the concentrations of human pancreatic secretory attemptpsin inhibitor (SPINK1) in various biological fluids. Contrary to other SPINK1 tests, this top-quality kit has been developed to provide the best performance for a specific species. Its sensitiveness and specificity make it ideal for research. Its high degree of accuracy and precision are only some of the benefits of the Boster Bio SPINK1 ELISA assay.

The SPINK1 ELISA Kit is easy to use and offers the highest sensitivity and reliability. OVCAR3 cells are cultivated in 10 cm dishes and grown overnight. The culture medium is complete. One control plate was saline-starved overnight using Peprotech. The cells were treated with rSPINK1 and 100 ng/ml of EGF. After 15 minutes the cells were then eliminated using 1% Triton-X solution. The protein concentrations were later determined. The protein samples were then examined using BCA and bicinchoninic acid tests. For QC, we used the aid of SpectraMax Multi Mode Microplate Reader. The samples with a concentration adjustment were placed on 4-20% gradient SDS gels before being transferred to nitrocellulose membranes.

Research on cell culture

An in vitro study of the expression levels of the SPINK1 marker revealed that cells exposed to multiple genotoxic agents displayed reduced levels of this marker. Furthermore, BLEO exposure did not confer a survival advantage on cells that have SPINK1 overexpression. The results confirm this theory, as SPINK1 is induced by several toxic agents. Therefore, cell-culture studies with the SPINK1 marker can be a useful method of studying the function of the NFKB pathway in cancer cells.

Although SPINK1 expression in colorectal and breast cancer carcinoma is comparable but it is associated with poor outcomes. Moreover, cancer cells expressing SPINK1 exhibit distinct pathological properties. SPINK1 is linked to activation of the c-Raf, MEK, and ERK pathways. However, the significance of SPINK1 in the progression of cancer is not fully understood.

Combination chemotherapy and stromal component targeted therapies is a viable method to decrease acquired resistance in patients with cancer. An anti-SPINK1 monoclonal antibody, (SPINK1 specific) is responsible for triggering the formation of inactive EGFR dimers and sequestering the ligand.

These studies suggest that BRAF mutations and SPINK1 overexpression is associated with poor prognosis. However mutations in SPINK1 don't appear to have a significant impact on prognosis. Both are important indicators in the field of cancer research. This is the first study of its kind to study the relationship between BRAF V600E and SPINK1 expression within cancer cells.

The SPINK1 protein is widely expressed in solid tumour stroma. Its levels in peripheral blood of patients suffering from cancer after chemotherapy show a negative correlation with the outcome. The results show that SPINK1 is an independent marker for damaged by treatment TME and its expression could serve as a clinical biomarker for monitoring and control of disease. However, further research is required to establish the role of SPINK1 in tumour progression.

Hypoxia-induced radioresistance to tumors

Recent research showed hypoxia-induced radioresistance to tumor radioresistance is easily mapped using SPINK1 marker. This marker is produced by cancer cells and has been demonstrated by the HIF-1 family to boost the resistance of tumor radioresistance. This marker can be used to predict how cancer cells are likely to react to chemotherapy.

The SPINK1 protein is closely related to EGF with a 50% resemblance. SPINK1 is a ligand for EGFR and activates EGFR signaling cascade. This is crucial for cell expansion and survival. SPINK1 triggers radioresistance via paracrine and EGFR dependent mechanisms. However SPINK1 does not display radioprotective activities when EGFR activation is reduced.

It is interesting to note that overexpression of the SPINK1 marker significantly enhanced the longevity of HeLa and DU145 cells in culture. These findings suggest that SPINK1 could function as a marker for hypoxia in tumors and may be a potential therapeutic target for radiosensitization. In tumors with hypoxic conditions, SPINK1 expression was also elevated in tumor cells.

The SpINK1 gene is a transcription factor found in the brain that regulates expression of nuclear EGFR and DNA-PK in cells. Overexpression of Twist1 in cancer cells enhances the radiation resistance of tumors and is related to poor prognosis. Hence, Twist1 is a potential molecular target for improving the effectiveness of radiation cancer therapy.

Furthermore, anemia treatment of mice increased the amount secreted SPINK1 mRNA and protein in tumor tissues. Plasma SPINK1 levels were significantly associated with tumor hypoxia and the volume of xenografted tumors, but they were not higher in non-tumor-bearing mice. These results indicate that SPINK1 is a result of tumor xenografts.

Neutralization of SPINK1

Boster Bio discovered that neutralization of SPINK1 marker causes an increase in the activity of MTs. These results are consistent with previous studies which have shown that SPINK1 is a key regulator of CRC's function. Furthermore, because SPINK1 is expressed in cancer cells, SPINK1 blockade might be an ideal therapeutic option. Furthermore, SPINK1 is a key regulator of MTs in several types of cells, such as breast cancer and colon cancer.

SPINK1 was first identified as a trypsin inhibitor. However, the systematic inhibition could cause adverse consequences. Further studies are needed to determine if SPINK1 is present in healthy pancreatic tissues. If it is, these findings could open an avenue to targeted cancer treatment. Additionally, further research is needed to better understand the difference between SPINK1 expression in pancreatic cancer cells and in normal pancreas tissue.

In the vivo environment, SPINK1 promotes tumor growth by increasing radioresistance in tumors. SPINK1 was found in tumors of DU145/SPINK1 mice who had breast cancer and also in the increased tumor growth after radiation therapy. These findings suggest that SPINK1 is an intrinsic hypoxia marker. The mechanism for this is not yet clear. However it is possible that tumors that express SPINK1 are radio-resistant and that anti-SPINK1 antibodies could prevent resistance from forming.

Hypoxia-induced hyperxia response gene activation regulates SPINK1 expression by increasing carbonic acide 9 (CA9). It also regulates the expression of genes within the hypoxia-response region in a HIF-dependent manner. HIF-a protein's stability is regulated by von Hippel-Lindau-containing E3 ubiquitin ligases and the 26S proteasome.

Susceptibility to cancer

The SPINK1 gene is involved in the regulation of several processes in cancer, including its proliferation, metastasis, transdifferentiation, and stemness. To discover new therapeutic strategies for this gene, it's necessary to have a deeper understanding of its functions. This review synthesizes the clinical and transcriptomic information on various types of cancer. To identify potential tumorigenesis sites The review also provides SPINK1 expression at single-cell levels.

The SPINK1 gene expression is correlated to CFTR. However mutations in this gene do not increase the likelihood of developing PC. The SPINK1 gene only is found in a small percentage of cancer patients. It is not a diagnostic indicator. The SPINK1 gene can be used to evaluate patients' cancer-related risk.

This gene is used to assess the risk of different cancers. The utility of this gene in early detection and the development of drugs has been proven through molecular analysis. The SPINK1 gene is affected in various types of cancers. The N34S variant is very common, and is responsible for various diseases. Boster Bio's laboratory has developed a brand new probe to detect the N34S variant.

The SPINK1 gene is an inhibitor of pancreatic secretory trypsin. It is secreted into pancreatic juice. It plays an important physiologic function in preventing premature activation. Although the mechanism of SPINK1 action is still unknown but it's a promising option for future research in this area. Patients who have had a history of prostate cancer have proved that the SPINK1 gene may influence the progress of cancer.