TACSTD2 or TROP2 is a transmembrane glycoprotein which epithelial cells express and which participates in cellular adhesion as well as cell proliferation and signal transduction processes. Lung epithelial cells and their progenitors produce the majority of TACSTD2 transcripts while the gene expression of TACSTD2 gets directly activated in lung epithelial cells following infection. Elevated levels of TACSTD2 expression function as a way to preserve or repair epithelial barrier integrity while aiding in lung tissue regeneration following infection or damage. Tumor research identifies TACSTD2 as a cancer stem cell marker which shows high expression levels across multiple solid tumors and links to cancer cell plasticity as well as tumor growth and metastatic behavior while influencing prognosis.
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Structure of TACSTD2
The TACSTD2 protein is built from 323 amino acids and weighs about 36–40 kDa before glycosylation increases its size. The membrane glycoprotein consists of a single spanning structure while its architecture includes several principal regions:
| Region |
Position |
Function |
| Extracellular domain |
Amino terminal (N-terminal) |
Contains EGF-like domain and cysteine-rich region, involved in ligand recognition, cell-cell adhesion and signal transduction |
| Transmembrane region |
Central |
Fixes protein on cell membrane, providing anchor for signal transduction |
| Intracellular tail |
Carboxyl terminal (C-terminal) |
Contains phosphorylation sites, can interact with intracellular signaling molecules, and regulate downstream signaling pathways |
Physiological Activity and Function of TACSTD2
TACSTD2 functions as a calcium signal transduction protein and shows primary expression in tumor cells. This protein operates as a membrane protein known both as GA733-2 and Trop2 while contributing critically to cellular development and physiological functions across multiple cell types.
Cell Signal Transduction
This protein triggers several signaling pathways including PI3K/Akt which leads to increased cell proliferation and survival. MAPK/ERK, regulating cell division and migration. β-catenin/Wnt, affecting stemness and epithelial-mesenchymal transition (EMT).
Cell Proliferation and Regeneration
The expression of TACSTD2 reaches high levels in both stem cells and epithelial cells undergoing regeneration. Tissue damage or infection triggers TROP2 to facilitate quick epithelial cell proliferation and re-epithelialization which speeds up the tissue repair process.
Maintaining Epithelial Barrier Integrity
TACSTD2 strengthens the intercellular junction structure while protecting the alveolar epithelial barrier against fluid leakage and pathogen invasion.
Activity Related to Tumorigenesis and Development
The expression of TACSTD2 peaks across multiple cancer types like lung cancer and breast cancer while showing strong links to EMT processes as well as cellular migration and invasion along with resistance to chemotherapy treatments.
Role of TACSTD2 in Lung Infection
In response to lung infections like viral or bacterial pneumonia epithelial cells and immune cells display substantial alterations in their gene expression patterns. Studies have found that during lung infection:
- Alveolar epithelial cells show a significant increase in TACSTD2 expression levels.
- The function of this biological process extends to the regulation of epithelial barrier integrity as well as inflammatory processes and tissue restoration.
- The elevated expression of this gene appears to play a role in both cell regeneration processes and immune system regulation following pathogen invasion.
Potential of TACSTD2 as Target
The gene TACSTD2 becomes more active in lung infections while possibly participating in inflammation and repair processes which positions it as a potential therapeutic target.
- Diagnostic marker: This molecule functions as a biomarker by indicating either the severity or pathological state of lung infections.
- Therapeutic target: The reduction of lung damage resulting from infection should be achievable through the inhibition or regulation of TACSTD2 function.
- Drug development: Cancer treatments using anti-TROP2 drugs including antibody-drug conjugates have potential application in lung disease therapies.
Fig 1. The immunohistochemical technique reveals Trop2 presence in paraffin-embedded sections from human, mouse, and pig lung tissues (Lenárt, S., et al. 2022).
TACSTD2 Gene Expression Level Increases in Lung Epithelial Cells Infection
The TACSTD2 gene produces TROP2, a transmembrane glycoprotein present in multiple epithelial tissues that regulates cell signaling alongside proliferation and repair functions. Inflammatory responses along with damage and repair processes affect lung epithelial cells. Research indicates TACSTD2 expression increases during these cellular processes which might be linked to subsequent biological outcomes.
Promote Epithelial Cell Regeneration and Repair
Through PI3K/Akt signaling pathway activation TROP2 promotes cell growth while speeding up the repair process of the damaged alveolar epithelium.
Enhance Barrier Function
TROP2 expression works to preserve cell-to-cell links and strengthen lung barrier function which prevents pathogens from entering.
Regulate Immune Response
Research demonstrates TROP2's role in controlling inflammatory factor discharge and impacting local immune microenvironments.
Future Research Directions
- Mechanism research: Study the molecular function of TACSTD2 during lung infection.
- Animal model verification: Examine the effect of lung injury following infection by using mice models with either knocked out or overexpressed genes.
- Clinical sample analysis: Determine how TACSTD2 levels correlate with both patient prognosis and the severity of disease.
- Targeted intervention experiment: The study aims to determine if blocking TACSTD2 activity will decrease lung inflammation and speed up repair processes.
TACSTD2 Upregulated in Infected Lungs and an Important Target
TACSTD2/TROP2 functions as a multifunctional transmembrane protein which features a unique structure along with strong signal transduction capability while serving as a key regulator in tissue repair processes and tumor biology. Experts now recognize TACSTD2 as an important factor in both infection response and repair processes in lung epithelial cells. While its upregulation functions as part of the inflammatory response it also likely serves as a crucial element in tissue self-protection and reconstruction processes. TACSTD2 functions as a molecular marker which indicates infection or early lung injury. Control of lung inflammation and promotion of tissue repair may be achievable through modulation of TROP2 expression or function. The progression of lung cancer links to TROP2 while research suggests possible ties between infection-inflammation-carcinogenesis processes.
References
- Lenárt, S., et al. TACSTD2 upregulation is an early reaction to lung infection. Scientific reports. 2022, 12(1): 9583.
- Kok, V., et al. Trop-2-Cells, Their Exosomal Cargo, and the Potential Impact on Diagnostics and Therapeutics in Breast Cancer: The Expanding Frontiers. Exploratory Research and Hypothesis in Medicine. 2023, 8(1): 81-85.
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