Xiaohui Chen

Relationship between human epididymal protein 4 and depth of tumor invasion, postoperative recurrence, and metastasis of epithelial epithelial ovarian cancer

AbstractThis study aimed to analyze the relationship between human epididymal protein 4 (HE4) and infiltration depth, postoperative recurrence, and metastasis of epithelial ovarian cancer (OVCA). Immunohistochemistry was used to detect the expression level of HE4 in cancer tissues and adjacent tissues of 90 patients with epithelial OVCA admitted to our hospital from May 2017 to January 2018. Cox regression was used to analyze the factors affecting the prognosis of epithelial OVCA. The relationship between HE4 and the prognosis of epithelial OVCA was analyzed by the receiver operating characteristic curve and Kaplan‐Meier survival curve. The positive expression rate of HE4 in epithelial OVCA was 85.56%, which was higher than 34.44% in adjacent tissues (p < 0.01). The International Federation of Gynecology and Obstetrics stage, infiltration depth, lymph node metastasis, postoperative recurrence and metastasis, and HE4 positivity were independent risk factors for the prognosis, and platinum‐based chemotherapy sensitivity was an independent protective factor for the prognosis of patients with epithelial OVCA (p < 0.05). The area under the curve of HE4 in diagnosing epithelial OVCA and predicting recurrence was 0.863 and 0.700, the sensitivity was 91.60% and 85.60%, and the specificity was 90.20% and 65.60%. The median progression‐free survival and overall survival were 26.1 and 30.2 months in HE4‐positive epithelial OVCA patients, while these were 31.4 and 35.6 months in HE4‐negative epithelial OVCA patients (p < 0.05). In conclusion, HE4 was highly expressed in epithelial OVCA tissues. Its expression level was related to the depth of tumor invasion, postoperative recurrence and metastasis, and other clinicopathological characteristics of patients with epithelial OVCA.

MALAT1 overexpression contributes to choriocarcinoma by binding with RBM10 and promoting p53 degradation

Choriocarcinoma (CC), a highly aggressive and malignant subtype of gestational trophoblastic disease (GTD), arises from the dysregulated proliferation of trophoblastic cells, which normally mediate placental development during pregnancy. This study aimed to characterize the expression and functional significance of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a nuclear-enriched long non-coding RNA, in CC pathogenesis. We analyzed MALAT1 expression levels in 30 normal placental villi, 46 hydatidiform moles (repressive subtype), and 52 CC specimens. To identify MALAT1-interacting proteins, we performed RNA antisense purification followed by immunoblotting, with subsequent validation via co-immunoprecipitation (Co-IP) and immunofluorescence (IF) assays. MALAT1 was significantly upregulated in CC tissues compared to controls. In vivo xenograft experiments further revealed that MALAT1 overexpression enhanced tumor growth. Mechanistically, we identified RNA-binding motif protein 10 (RBM10), a key spliceosomal regulator, as a novel MALAT1-binding partner. Strikingly, MALAT1 promoted p53 protein degradation without affecting its transcriptional levels, and this oncogenic effect was mediated through an RBM10-dependent mechanism. In conclusion, our findings establish MALAT1 as a critical oncogenic driver in CC, functioning through its interaction with RBM10 to destabilize p53 and accelerate tumor progression. These insights highlight the potential of the MALAT1-RBM10-p53 axis as a therapeutic target in CC.