The protease TASP1 remains highly conserved throughout evolution because it breaks down MLL and controls homologous gene expression while also playing a role in cancer development. TASP1 blocks aspartase 1 activity to prevent the growth of both breast and brain cancer cells and delivers therapeutic benefits. Research demonstrates that TASP1 shows high expression in cancer cells while its downregulation leads to increased apoptosis of cancer cells and reduces their proliferation ability. TASP1 significantly influences the development of numerous cancers particularly gastric cancer and breast cancer through its established capability to stimulate cell proliferation and migration.
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Threonine Aspartase 1 (TASP1) Participates in Gastric Cancer Progression
TASP1 functions as an endopeptidase by using its asparaginase-2 homology domain to identify and break down substrates containing a conserved aspartate peptide motif at the P1 position. Although TASP1 does not fit the traditional profile of an oncogene it facilitates cancer development through the cleavage of MLL and TFIIA making it a viable target for anticancer drugs.
Promote Cell Proliferation
The proliferation of gastric cancer cells increases due to TASP1 which activates proteins through cleavage that regulate cell cycle progression. Research has shown that TASP1 speeds up the cell cycle while enabling rapid cancer cell multiplication through control of c-Myc and Cyclin D1 gene expression.
Promote Cell Migration and Invasion
The metastatic potential of gastric cancer cells increases through TASP1's influence on epithelial-mesenchymal transition pathways which leads to reduced cell adhesion and better cancer cell movement. The specific mechanism functions through the control of EMT-related proteins including Snail, E-cadherin, and N-cadherin.
Possible Signaling Pathways
- Notch signaling pathway: Notch receptor precursor cleavage by TASP1 regulates Notch signaling which affects gastric cancer cells' proliferation and invasion.
- PI3K/AKT/mTOR pathway: TASP1 enhances cancer cell survival and migration through activation of the PI3K/AKT/mTOR pathway.
Fig 1. TASP1 is overexpressed in GC tissues and GC cells (Wan, X., et al. 2021)
Threonine Aspartase 1 (TASP1) Functions as A Key Enzyme in Breast Cancer Biology
The enzyme Threonine aspartase 1 (TASP1lation and apoptosis signaling depend on this relationship. Scientific research into breast cancer is increasingly focusing on the role of TASP1. Research indicates that TASP1 could impact tumor cell proliferation through its regulation of cell cycle-related protein levels. The growth rate of tumor cells is affected by alterations in the expression level of this enzyme. Research suggests that TASP1 has a regulatory effect on tumor cell apoptosis. TASP1 influences breast cancer cells' response to chemotherapy and radiotherapy through its regulatory actions on apoptosis-related signaling pathways.
Promote Breast Cancer Cell Growth
Research shows that TASP1 controls the alternative splicing process of crucial genes HOXA9 and HOXA10 which are important in breast cancer development. The proliferation index (Ki-67) of breast cancer demonstrates a strong correlation with elevated TASP1 expression levels.
Promote Breast Cancer Metastasis
Matrix metalloproteinases (MMPs) and EMT contribute to breast cancer metastasis. The invasive potential of cancer cells can be boosted by TASP1 through its regulatory effect on these biological factors. The expression of TASP1 in TNBC (triple-negative breast cancer) shows increased levels which correlate with both lymph node metastasis and distant metastasis.
Key Pathways
- Wnt/β-catenin pathway: Through this pathway TASP1 may control breast cancer cell proliferation and migration.
- JAK/STAT3 pathway: TASP1 enhances the invasive potential of breast cancer cells via this signaling pathway.
TASP1 as A Potential Therapeutic Target
The enzyme TASP1 (Taspase 1) plays a crucial role in cellular protein processing and regulation. TASP1 functions primarily by cutting specific proteins within various cellular signaling pathways. Recent scientific research demonstrates that TASP1 is linked to the development and emergence of several diseases such as cancer and neurodegenerative disorders. TASP1 has emerged as a potential therapeutic target for disease treatment.
| TASP1 inhibitors |
Research reveals that TASP1-targeting small molecule inhibitors reduce cancer cell proliferation as well as migration. |
| Combination therapy |
Cancer treatment results improve when TASP1 inhibitors work in combination with chemotherapy drugs such as paclitaxel and cisplatin or targeted medicines like Herceptin. |
TASP1 Supports both growth and movement in gastric cancer and breast cancer via various signaling mechanisms
TASP1 functions as an essential element in processes of tumor metastasis and invasion. TASP1 influences tumor cell migration by controlling both cell-cell adhesion and matrix degradation processes.
TASP1 increases gastric cancer cell growth and movement but when TASP1 levels decrease this leads to reduced cell growth and more E-cadherin while less N-cadherin stops cell movement.
Expression levels of TASP1 rise in breast cancer tissues and cell lines and its inhibition stops breast cancer growth and spread through ESR1 blockade.
Breast and gastric cancer cells proliferate and migrate more effectively because TASP1 activates multiple signaling pathways and its elevated levels predict worse tumor development and patient survival outcomes. TASP1 serves as a possible biomarker and therapeutic target that offers a novel approach to precision medicine for gastric cancer and breast cancer treatment.
References
- Wan, X., et al. TASP1 promotes proliferation and migration in gastric cancer via EMT and AKT/P‐AKT pathway. Journal of Immunology Research. 2021, 1: 5521325.
- Xiong, F., et al. TASP1 promotes the proliferation and metastasis of breast cancer by up-regulating ESR1. 2024.
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