Abstract
Maintaining a robust epithelial barrier requires the accumulation of tight junction proteins, LSR/angulin-1 and tricellulin, at the tricellular contacts. Alterations in the localization of these proteins temporarily cause epithelial barrier dysfunction, which is closely associated with not only physiological differentiation but also cancer progression and metastasis. In normal human endometrial tissues, the endometrial cells undergo repeated proliferation and differentiation under physiological conditions. Recent observations have revealed that the localization and expression of LSR/angulin-1 and tricellulin are altered in a menstrual cycle-dependent manner. Moreover, it has been shown that endometrial cancer progression affects these alterations. This review highlights the differences in the localization and expression of tight junction proteins in normal endometrial cells and endometrial cancers and how they cause functional changes in cells.
Highlights
The endometrium is a regenerative tissue in which the cells undergo proliferation and differentiation depending on the levels of estrogen, progesterone, or various cytokines
Recent studies have revealed that the localization of tricellular tight junction proteins, tricellulin and LSR/angulin-1, to tricellular contacts is required for epithelial barrier maturation based on the proper localization of OCLN and CLDNs [7]
Various cancerous malignancies are associated with changes in the expression and localization of bicellular tight junction proteins and tricellular tight junction proteins. These findings suggested that tricellular tight junction proteins may interact closely with bicellular junctions during malignant transformation in response to reduction of the barrier function
Summary
The endometrium is a regenerative tissue in which the cells undergo proliferation and differentiation depending on the levels of estrogen, progesterone, or various cytokines. It has been shown that robust epithelial barrier formation requires localization of these tight junction proteins at the subapical region by analyzing primary cultured normal human endometrial cells. Recent studies have revealed that the localization of tricellular tight junction proteins, tricellulin and LSR/angulin-1, to tricellular contacts is required for epithelial barrier maturation based on the proper localization of OCLN and CLDNs [7]. A recent study demonstrated that tricellulin localized in the subapical region during the endometrial secretory phase, whereas LSR was broadly distributed to the lateral region [8]. Analysis using primary cultured normal human endometrial cells revealed that localization of LSR to the tricellular contacts is required for the formation of mature epithelial polarity with sufficient barrier function.
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