Xiaotong Sun

Knockdown of Trop2 inhibits proliferation and migration and induces apoptosis of endometrial cancer cells via AKT/β‐catenin pathway

Endometrial cancer (EC) is the most common gynaecologic malignancy in western countries and has been reported to account for about 7% of female malignant tumours and 20% to 30% of female genital system malignant tumours. Accumulating evidence showed the expression of human trophoblast cell surface antigen 2 (Trop2) was abnormal in many cancers; however, the expression and role of Trop2 in EC are not clear. The Trop‐2 protein expression was detected by western blot in EC cells. Cell proliferation, apoptosis, and migration were measured by CCK‐8, flow cytometry, and Transwell assay, respectively. The epithelial mesenchymal transition (EMT) and AKT/β‐catenin signalling pathway–related proteins in EC cell lines were detected by western blot assay following Trop2 gene silencing. The present study revealed that the Trop2 protein was highly expressed in EC cell lines compared with human endometrial epithelial cells. The Trop2 mRNA and protein were obviously decreased following transfection with Trop2‐siRNA sequence in KLE and Ishikawa cells. Meanwhile, Trop2 gene silencing in KLE and Ishikawa cells strongly inhibited cell proliferation and migration and increased cell apoptosis. Investigation into the molecular mechanism indicated that the Trop2 gene silencing suppressed EMT and AKT/β‐catenin signalling pathway activation.Significance of the studyThese findings suggested that Trop2 silencing inhibited EC cell proliferation and migration and promoted cell apoptosis. The mechanism might be related to the inhibition of the AKT/β‐catenin signalling pathway in EC cells. Therefore, Trop2 may be a potential therapeutic target for the treatment of EC.

Primary vaginal adenocarcinoma as a radiation-associated secondary malignancy: A case report and comprehensive literature review

Rationale: Primary vaginal adenocarcinoma (PVA) is an exceptionally rare malignancy, with most cases historically linked to in utero diethylstilbestrol (DES) exposure. Non–DES-associated PVA following definitive chemoradiotherapy for cervical cancer is extremely uncommon, and no standardized management protocol exists. This case illustrates a rare instance of radiation-associated PVA and highlights therapeutic considerations in previously irradiated pelvic fields. Patient concerns: A 53-year-old postmenopausal woman presented with intermittent vaginal bleeding occurring 5 years after radical hysterectomy and adjuvant chemoradiotherapy for stage IIA2 cervical squamous cell carcinoma. Diagnoses: Colposcopy-guided biopsies of the vaginal anterior wall revealed glandular architecture with cytological atypia. Immunohistochemistry demonstrated CK7(+), CK8/18(+), CEA(+), PAX8(−), ER(−), PR(−), p16 patchy weak negative, and wild-type p53. Systemic workup excluded metastatic disease, supporting the diagnosis of PVA (non–DES-associated, radiation-related). Interventions: In view of prior pelvic irradiation, the multidisciplinary team recommended dose-adjusted paclitaxel–cisplatin combination chemotherapy. Six cycles were administered, tailored to minimize cumulative toxicity. Outcomes: At 6-month follow-up, imaging studies confirmed complete clinical remission, with no locoregional recurrence or distant metastases. Lessons: This report underscores the potential for radiation-induced secondary vaginal adenocarcinoma in cervical cancer survivors, even after prolonged remission. Vigilant long-term surveillance, including annual vaginal cytology and targeted biopsies, is critical for early detection. Individualized therapeutic strategies – integrating prior treatment history, immunohistochemical profiling, and consideration of molecular alterations – are essential for optimizing outcomes in this rare patient population.