MTSS1

Official Full Name

MTSS I-BAR domain containing 1

Organism

Homo sapiens

GeneID

9788

Background

Enables actin monomer binding activity; identical protein binding activity; and signaling receptor binding activity. Predicted to be involved in several processes, including adherens junction maintenance; positive regulation of actin filament bundle assembly; and renal tubule development. Predicted to act upstream of or within several processes, including actin filament polymerization; bone mineralization; and magnesium ion homeostasis. Located in actin cytoskeleton. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

MIM; MIMA; MIMB;

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Detailed Information

MTSS1 (metastasis suppressor 1), also known as MIM (missing in metastasis), was discovered by Lee et al. in the study of bladder cancer metastasis and was originally defined as a metastasis suppressor gene. MTSS1 can play an important role in the biological behavior of malignant tumors by regulating the infiltration and metastasis of actin involved tumors in multiple ways.

MTSS1 Function

The full-length cDNA of MTSS1 is MIM-B, which has multiple functional motifs, including the N-terminal IRSp53/MIM homology domain (IMD), the coiled-coil domain, the lysine-rich domain (LRD) , and the Ser-rich domain (SRD), Pro-rich domain (PRD) and Wiskott-Aldrich syndrome protein homology2 (WH2) domain at the C-terminus. The most studied are IMD and WH2 domain. In vitro, MIM, one of the MTSS1 splice variants, inhibits actin filament nucleation, which is located in the WH2 domain at the C-terminus.

Figure 1. MTSS1 and SCAMP1 cooperate to prevent invasion in breast cancer. (Vadakekolathu, J., 2018)

MTSS1 is primarily located between cells and is closely related to actin, which plays a role in the formation, strengthening, and maintenance of intercellular connections. Arp2/3 regulates reversible breakdown, cross-linking, and reassembly of actin filaments, mediating actin nucleation, while MTSS1 promotes Arp2/3 mediated actin filament assembly and binds to cell membrane and actin Monomers to maintain the integrity of epithelial cells.

MTSS1 antagonizes hepatocyte growth factor-mediated cell dissemination and immobilizes most E-cadherin junctions, thereby slowing tumor metastasis. In addition, MTSS1 inhibits tumor cell migration by enhancing the strength of intercellular junctions and specifically consolidating intercellular E-cadherin inhibition of epithelial-mesenchymal transition. Deletion of MTSS1 can cause actin cytoskeletal disruption between cell junctions and increase cell depolymerization, thereby promoting tumor metastasis.

Studies have found that high expression of MTSS1 on the cell surface increases Erk1 /2 phosphorylation induced by epidermal growth factor, further extending downstream intracellular signaling. In addition, high expression of MTSS1 also delays the activation of protein kinase B (Ark). Cellular epidermal growth factor receptor signaling regulates the formation of intercellular junctions, suggesting that MTSS1-driven EGF signaling may directly increase the formation of intercellular junctions. In vivo, high expression of MTSS1 in metastatic tumors leads to increased keratinization and decreased proliferation, which also supports the inhibition of cell proliferation by MTSS1 in high-density cells.

MTSS1 and Tumor

The degree of differentiation of bladder transitional cell carcinoma is positively correlated with the expression of MIM. The expression rate of MIM is higher in tumor tissues with higher degree of differentiation, but lower in tumor tissues with lower differentiation. Studies have shown that MIM is rarely expressed in EJ138, T24 and RT112 cell lines in bladder cancer cell lines. Overexpression of MIM is inversely related to the growth and cell adhesion of bladder cancer cell lines in vitro, but does not affect its ability to invade and metastasize.

The expression of MTSS1 in 98 NSCLC tissues and corresponding adjacent tissues was detected by immunohistochemistry. The positive expression rate of MTSS1 in cancer tissues was lower than that in adjacent tissues. The expression of MTSS1 was not associated with gender, age, degree of differentiation, and pathological type, but was associated with lymph node metastasis and N stage. The median overall survival of MTSS1 positive expression was 40. 9 months, higher than the negative expression of 21. 5 months.

References:

Vadakekolathu, J., Aljuboori, S. I. K. , Johnson, C. , Schneider, A. , Magdalena Elżbieta Buczek, & Biase, A. , et al. (2018). Mtss1 and scamp1 cooperate to prevent invasion in breast cancer. Cell Death & Disease, 9(3).
Taylor, M. D. , Bollt, O. , Iyer, S. C. , & Robertson, G. P. . (2017). Metastasis suppressor 1 (mtss1) expression is associated with reduced in-vivo metastasis and enhanced patient survival in lung adenocarcinoma. Clinical & Experimental Metastasis.
Peng, D. U. , Wang, S. , Tang, X. , Chao, A. N. , & Jiang, W. G. . (2017). Reduced expression of metastasis suppressor-1 (mtss1) accelerates progression of human bladder uroepithelium cell carcinoma. Anticancer research, 37(8), 4499-4505.

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