Low-grade adenosquamous carcinoma (LGASC) is a rare invasive tumor that occurs in breast parenchyma. It has previously only been reported in females. Herein, we describe the case of a 52-year-old male who presented with a palpable mass in his right axilla that he reported had been present for 20-years. This is the first report of a male patient with LGASC. Core needle biopsy pathology revealed a benign mass of mammary origin, but its type was initially misdiagnosed. It was only correctly identified via postoperative pathology after local excision, which indicated that the mass exhibited the typical pathological characteristics of LGASC. Immunohistochemical analysis revealed positive expression of estrogen receptor, which was inconsistent with the typical "triple-negative" immunophenotype of LGASC. After resection of the mass the patient was advised to participate in regular outpatient follow-up. In conclusion, LGASC should be considered in male patients with a mass lesion in their breast or axilla, even when core needle biopsy indicates a benign mass of breast origin. One-stage local resection is recommended for the treatment of male patients with LGASC, but it is crucial to ensure that the margins are negative and postoperative adjuvant radiotherapy is not recommended.

Background Aquaporin 3 (AQP3) and Cellular-mesenchymal to epithelial transition factor (c-Met) are both overexpressed in human breast cancer and highly related to proliferation and migration. However, it is still unclear whether c-Met is associated with AQP3. The study objective was to explore the relationship between c-Met and AQP3 in human breast cancer. Methods We used immunohistochemistry to determine the expression of AQP3 and c-Met in breast cancer tissue specimens and analysed whether there was any correlation between the two molecules. Real-time quantitative polymerase chain reaction and Western blotting were used to detect AQP3 expression in MCF-7 and MDA-MB-231 cells after human hepatocyte growth factor (hHGF) treatment and/or transfection with c-Met silencing small interfering (si)RNA. Additionally, cell migration was examined with a wound scratch assay. Results Based on the immunohistochemical results combined with the clinicopathological data of 59 breast cancer patients, c-Met exhibited a significant correlation with AQP3 in breast cancer tissue. Studies have shown that hHGF can increase c-Met phosphorylation, and we discovered that the hHGF-induced increase in AQP3 expression was dose dependent. However, after reducing c-Met expression with c-Met-specific siRNA, AQP3 expression decreased accordingly. Additionally, the wound scratch assay showed that AQP3-specific siRNA or c-Met-specific siRNA significantly inhibited breast cancer cell migration, which was promoted by hHGF. Conclusions Our study indicated that AQP3 expression was regulated by c-Met in human breast cancer. These discoveries may help us comprehend the mechanisms underlying breast cancer development and invasion and offer another possibility for targeted treatment of breast cancer.