Abstract
Oral carcinogenesis is complex and multi-step process, which results from various deleterious habits, multiple environmental factors and genetic susceptibility. CLDN-1 expression is regulated oncogenic Wnt/B-catenin transduction pathway. They recruit matrix metalloproteinases (MMPs) on the cell surface to achieve elevated focal concentrations and eventual activations of proMMP2. These collagenases are responsible for the breakdown of extracellular matrix proteins and thus facilitate invasion and spread of malignant cells. Reduced cell-cell adhesion is associated with loss of contact inhibition of proliferation. This allows escape from growth control signals and triggers carcinogenesis. Significant correlation was observed between histopathological grade of the tumor with the localization and immunostaining intensity of CLDN-1. Determination of localization of CLDN-1 for a particular patient may be important to decide site (cytoplasmic or nuclear) for targeting CLDN-1. This targeted drug therapy for CLDN-1 may prevent worsening of the disease in the patient, resulting in better prognosis.
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