Key result
MIEN1 is overexpressed in multiple human cancers and promotes tumor metastasis and invasion through post-translational modifications and interactions with signaling pathways like PI3K/Akt and NF-kB.
Why the study?
Tumor metastasis accounts for numerous cancer-related fatalities worldwide, prompting the need to review the structure, function, and role of the membrane-associated protein MIEN1 in cancer progression.
This review highlights the structure, function, and emerging role of MIEN1 as a novel therapeutic target in cancer cell invasion and metastasis.
Answers are grounded in this paper and cite their sources.
MIEN1 should not yet guide clinical decisions; leaves open its validation as a therapeutic target in prospective trials.
Tumor metastasis is a sequential event accounting for numerous cancer-related fatalities worldwide. The process of metastasis serially involves invasion, intravasation, extravasation, and tumor growth at the secondary site. Migration and invasion enhancer 1 (MIEN1) is a membrane associated protein overexpressed in various human cancers. Biological activity of MIEN1 is driven by geranylgeranyltransferase-I mediated prenylation at CAAX motif and methylation of the prenylated protein that anchors MIEN1 into the cellular membrane. Post-translationally modified MIEN1 interacts with Syk kinase and Annexin A2 protein; polymerizes G-actin and stabilizes F-actin filament; induces focal adhesion kinase phosphorylation and decrease cofilin phosphorylation implicated in both invasion and metastasis of different cancer types. In the present review, we discuss the structure, function, and involvement of MIEN1 in cancer progression. We also highlight the future prospects of MIEN1 as an emerging molecule and novel target in cancer cell invasion and metastasis.
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Kushwaha et al. (2019) conducted a review in Cancer. MIEN1 was evaluated. MIEN1 is overexpressed in multiple human cancers and promotes tumor metastasis and invasion through post-translational modifications and interactions with signaling pathways like PI3K/Akt and NF-kB.
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