Xinyu Xu

A case of ovarian Teratoma with nephroblastoma presenting abdomen metastasis

AbstractBackgroundTeratoma with nephroblastoma (TWN) is an extremely rare condition. Since 1984, only 45 reported cases have been identified. To our knowledge, there have been only two cases of TWN of ovarian origin.Case presentationWe described a case of ovarian TWN who presented to us with painless abdominal masses 6 months after undergoing right ovarian cystectomy. The tumor had spread to the abdomen due to spontaneous rupture of the ovarian cyst and failure to undergo chemotherapy. Microscopically, the ovarian mass exhibited the typical components of a mature cystic teratoma. The tumors found in both the ovary and abdomen contained the nephroblastoma components and were strongly positive for WT‐1. The patient was advised to undergo chemotherapy and she was lost to follow‐up.ConclusionA careful histological examination is necessary for an accurate diagnosis, which is based on morphology and extensive immunohistochemical studies. According to the literature, surgical excision alone seems reasonable as the prognosis of TWN is considered to be good. However, due to the spontaneous rupture of the ovarian cyst, chemotherapy of the patient after the first surgery was necessary in our case. Therefore, additional case studies are needed to clarify the standardized treatment of TWN.

KCMF1 promotes malignant progression by NXN ubiquitin-dependent degradation in ovarian cancer.

Ovarian cancer, one of the most lethal gynecologic malignancies, exhibits marked tumor heterogeneity. Potassium channel modulatory factor 1 (KCMF1), a RING zinc-finger protein with E3 ubiquitin ligase activity, has been implicated in tumorigenesis. However, the role of KCMF1 in ovarian cancer remains unclear. In this study, we found that KCMF1 was up-regulated in ovarian cancer tissues and that high KCMF1 expression correlated with poor survival of patients. Functional assays revealed that KCMF1 knockdown suppressed cell viability, hampered cell cycle progression, and inhibited proliferation in ovarian cancer cells. Moreover, silencing KCMF1 inhibited epithelial-mesenchymal transition (EMT), migration, and invasion in vitro. In vivo experiments confirmed that KCMF1 knockdown inhibited tumor growth and metastasis in nude mice. Conversely, KCMF1 overexpression had opposite effects in vitro and in vivo. IP-LC/MS and Label-free proteomic analysis identified nucleoredoxin (NXN), a multifunctional redox-active protein, as a potential substrate of KCMF1. Silencing NXN facilitated cell proliferation, migration, and invasion through activating the β-catenin signaling pathway. Mechanistically, we discovered that KCMF1 interacted with NXN and facilitates its degradation through K63-linked ubiquitination, thereby reducing NXN expression. Taken together, our study showed that KCMF1 promotes ovarian cancer progression through NXN, and KCMF1 might be a novel target for ovarian cancer therapy.