Endometrial carcinoma (EC) is the most common gynecological malignancy, with increasing incidence linked to rising risk factors. This retrospective observational study investigates the role of the Androgen Receptor (AR) in EC aggressiveness, its correlation with other prognostic markers, and its potential therapeutic implications. A total of 143 cases of EC treated with hysterectomy were analyzed for AR expression and its association with clinicopathological and molecular markers, including estrogen receptor (ER), progesterone receptor (PR), Ki-67, p53, β-catenin, E-cadherin, Bcl-2, Cyclin D1, and mismatch repair (MMR) status. AR expression was significantly higher in low-grade endometrioid carcinoma (LGEC) compared to high-grade endometrioid carcinoma (HGEC) and other high-risk histologies (p = 0.015), suggesting a role in less aggressive tumor phenotypes. AR strongly correlated with ER and PR (p < 0.0001), indicating shared regulatory pathways. A borderline association with tumor-infiltrating lymphocytes (TILs) suggests a potential role in immune response. However, AR expression did not significantly correlate with markers of proliferation (Ki-67) or tumor suppression (p53), nor with β-catenin, E-cadherin, Bcl-2, Cyclin D1, or MMR status. These findings support AR as a prognostic marker in hormone-responsive EC subtypes and suggest that AR-targeted therapies could be beneficial, particularly in ER/PR-negative tumors. The study highlights the potential integration of AR status into molecular profiling, aiding in personalized treatment strategies for improved patient outcomes in EC management.