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1.
FASEB J ; 38(13): e23772, 2024 Jul 15.
Article in English | MEDLINE | ID: mdl-38963337

ABSTRACT

Ovarian cancer is one of the most common gynecologic malignancies that has a poor prognosis. THUMPD3-AS1 is an oncogenic long noncoding RNA (lncRNA) in several cancers. Moreover, miR-320d is downregulated and inhibited proliferation in ovarian cancer cells, whereas ARF1 was upregulated and promoted the malignant progression in epithelial ovarian cancer. Nevertheless, the role of THUMPD3-AS1 in ovarian cancer and the underlying mechanism has yet to be elucidated. Human normal ovarian epithelial cells (IOSE80) and ovarian cancer cell lines (CAVO3, A2780, SKOV3, OVCAR3, and HEY) were adopted for in vitro experiments. The functional roles of THUMPD3-AS1 in cell viability and apoptosis were determined using CCK-8, flow cytometry, and TUNEL assays. Western blot was performed to assess the protein levels of ARF1, Bax, Bcl-2, and caspase 3, whereas RT-qPCR was applied to measure ARF1 mRNA, THUMPD3-AS1, and miR-320d levels. The targeting relationship between miR-320d and THUMPD3-AS1 or ARF1 was validated with dual luciferase assay. THUMPD3-AS1 and ARF1 were highly expressed in ovarian cancer cells, whereas miR-320d level was lowly expressed. THUMPD3-AS1 knockdown was able to repress cell viability and accelerate apoptosis of OVCAR3 and SKOV3 cells. Also, THUMPD3-AS1 acted as a sponge of miR-320d, preventing the degradation of ARF1. MiR-320d downregulation reversed the tumor suppressive function induced by THUMPD3-AS1 depletion. Additionally, miR-320d overexpression inhibited ovarian cancer cell viability and accelerated apoptosis, which was overturned by overexpression of ARF1. THUMPD3-AS1 inhibited ovarian cancer cell apoptosis by modulation of miR-320d/ARF1 axis. The discoveries might provide a prospective target for ovarian cancer treatment.


Subject(s)
ADP-Ribosylation Factor 1 , Apoptosis , Gene Expression Regulation, Neoplastic , MicroRNAs , Ovarian Neoplasms , RNA, Long Noncoding , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , Female , Ovarian Neoplasms/genetics , Ovarian Neoplasms/pathology , Ovarian Neoplasms/metabolism , Apoptosis/genetics , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Cell Line, Tumor , ADP-Ribosylation Factor 1/metabolism , ADP-Ribosylation Factor 1/genetics , Cell Proliferation
2.
Arch Gynecol Obstet ; 310(1): 561-569, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38683394

ABSTRACT

PURPOSE: This study aimed to evaluate the clinical efficacy and safety of argon plasma coagulation (APC) therapy and interferon therapy in patients with grade I and II vaginal intraepithelial neoplasia (VaIN). METHODS: A total of 112 patients with VaIN were diagnosed via colposcopy-induced biopsy and classified into the APC group (n = 77) and interferon group (n = 35). Clinical data including age, grade, symptoms, historical or concomitant neoplasia of the lower genital tract, indications for hysterectomy, pregnancy history, cytology, human papillomavirus (HPV) subtype, treatment modalities, and clinical outcomes were analyzed, retrospectively. Complications and clinical outcomes were assessed at 6- and 12-month follow-ups. RESULTS: There was no significant difference in the HPV clearance rate between the APC (53.42%) and interferon (33.33%) groups at 6 months after treatment. However, the 12-month follow-up of the APC group showed a significantly higher HPV clearance rate as compared to the interferon group (87.67% vs. 51.52%, P < 0.05). The APC group exhibited a significantly higher cure rate (79.22% vs. 40.0%) and lower persistence rate (12.99% vs. 37.14%) than the interferon group (P < 0.05). Adverse reaction analysis revealed that the primary reaction in the APC group was vaginal drainage, in contrast to the increased vaginal discharge in the interferon group; though the difference was significant (68.83% vs. 28.57%, P < 0.05), no serious complications were observed. CONCLUSIONS: Treatment with APC is a safe and more effective procedure against VaIN I and II, compared to interferon. APC may serve as a viable alternative to other physiotherapies.


Subject(s)
Argon Plasma Coagulation , Carcinoma in Situ , Vaginal Neoplasms , Humans , Female , Retrospective Studies , Vaginal Neoplasms/drug therapy , Vaginal Neoplasms/virology , Vaginal Neoplasms/surgery , Vaginal Neoplasms/therapy , Adult , Middle Aged , Carcinoma in Situ/drug therapy , Carcinoma in Situ/surgery , Carcinoma in Situ/therapy , Carcinoma in Situ/virology , Carcinoma in Situ/pathology , Papillomavirus Infections/complications , Papillomavirus Infections/therapy , Treatment Outcome , Interferons/therapeutic use , Colposcopy , Combined Modality Therapy
3.
Zhong Nan Da Xue Xue Bao Yi Xue Ban ; 48(6): 941-946, 2023 Jun 28.
Article in English, Chinese | MEDLINE | ID: mdl-37587081

ABSTRACT

Primary endometrioid adenocarcinoma of the rectovaginal septum is rare. Its pathogenesis is not clear and there is no standard treatment. One patient with endometrioid adenocarcinoma of the rectovaginal septum arising from deep infiltrative endometriosis was admitted to Qingdao Municipal Hospital. The patient presented with incessant menstruation and abdominal distension. She had bilateral ovarian endometriotic cystectomy 6 years ago. Imaging findings suggested a pelvic mass which might invade the rectovaginal septum. Pathological results of primary surgery confirmed endometrioid carcinoma of the pelvic mass arising from the rectovaginal septum. Then she had a comprehensive staged surgery. Postoperative chemotherapy was given 6 times. No recurrence or metastasis was found during the 2-year follow-up. The possibility of deep infiltrating endometriosis and its malignant transformation should be considered in the differential diagnosis of a new extragonadal pelvic lesion in a patient with a history of endometriosis, which would avoid misdiagnosis and missed diagnosis.


Subject(s)
Carcinoma, Endometrioid , Rectal Neoplasms , Vaginal Neoplasms , Female , Humans , Carcinoma, Endometrioid/diagnostic imaging , Carcinoma, Endometrioid/drug therapy , Carcinoma, Endometrioid/pathology , Carcinoma, Endometrioid/surgery , Endometriosis/pathology , Endometriosis/surgery , Rectal Neoplasms/diagnostic imaging , Rectal Neoplasms/drug therapy , Rectal Neoplasms/pathology , Rectal Neoplasms/surgery , Vaginal Neoplasms/diagnostic imaging , Vaginal Neoplasms/drug therapy , Vaginal Neoplasms/pathology , Vaginal Neoplasms/surgery , Diagnosis, Differential
4.
PeerJ ; 9: e11375, 2021.
Article in English | MEDLINE | ID: mdl-33987033

ABSTRACT

BACKGROUND: Ovarian cancer is one of the leading causes of female deaths worldwide. Ovarian serous cystadenocarcinoma occupies about 90% of it. Effective and accurate biomarkers for diagnosis, outcome prediction and personalized treatment are needed urgently. METHODS: Gene expression profile for OSC patients was obtained from the TCGA database. The ESTIMATE algorithm was used to calculate immune scores and stromal scores of expression data of ovarian serous cystadenocarcinoma samples. Survival results between high and low groups of immune and stromal score were compared and differentially expressed genes (DEGs) were screened out by limma package. The Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and the protein-protein interaction (PPI) network analysis were performed with the g:Profiler database, the Cytoscape and Search Tool for the Retrieval of Interacting Genes (STRING-DB). Survival results between high and low immune and stromal score groups were compared. Kaplan-Meier plots based on TCGA follow up information were generated to evaluate patients' overall survival. RESULTS: Eighty-six upregulated DEGs and one downregulated DEG were identified. Three modules, which included 49 nodes were chosen as important networks. Seven DEGs (VSIG4, TGFBI, DCN, F13A1, ALOX5AP, GPX3, SFRP4) were considered to be correlated with poor overall survival. CONCLUSION: Seven DEGs (VSIG4, TGFBI, DCN, F13A1, ALOX5AP, GPX3, SFRP4) were correlated with poor overall survival in our study. This new set of genes can become strong predictor of survival, individually or combined. Further investigation of these genes is needed to validate the conclusion to provide novel understanding of tumor microenvironment with ovarian serous cystadenocarcinoma prognosis and treatment.

5.
Gynecol Oncol ; 149(2): 248-255, 2018 05.
Article in English | MEDLINE | ID: mdl-29572030

ABSTRACT

OBJECTIVE: Human papillomavirus (HPV) infection is the primary cause of cervical cancer. HPV-mediated immune alterations are known to play crucial roles in determining viral persistence and host cell transformation. We sought to thoroughly understand HPV-directed immune alterations in cervical cancer by exploring publically available datasets. METHODS: 130 HPV positive and 7 HPV negative cervical cancer cases from The Cancer Genome Atlas were compared for differences in gene expression levels and functional enrichment. Analyses for copy number variation (CNV) and genetic mutation were conducted for differentially expressed immune genes. Kaplan-Meier analysis was performed to assess survival and relapse differences across cases with or without alterations of the identified immune signature genes. RESULTS: Genes up-regulated in HPV positive cervical cancer were enriched for various gene ontology terms of immune processes (P=1.05E-14~1.00E-05). Integrated analysis of the differentially expressed immune genes identified 9 genes that displayed either CNV, genetic mutation and/or gene expression changes in at least 10% of the cases of HPV positive cervical cancer. Genomic amplification may cause elevated levels of these genes in some HPV positive cases. Finally, patients with alterations in at least one of the nine signature genes overall had earlier relapse compared to those without any alterations. The altered expression of either TFRC or MMP13 may indicate poor survival for a subset of cervical cancer patients (P=1.07E-07). CONCLUSIONS: We identified a novel immune gene signature for HPV positive cervical cancer that is potentially associated with early relapse of cervical cancer.


Subject(s)
Human papillomavirus 16/physiology , Human papillomavirus 18/physiology , Papillomavirus Infections/immunology , Uterine Cervical Neoplasms/immunology , Uterine Cervical Neoplasms/virology , Case-Control Studies , Female , Human papillomavirus 16/genetics , Human papillomavirus 16/immunology , Human papillomavirus 18/genetics , Human papillomavirus 18/immunology , Humans , Mutation/immunology , Papillomavirus Infections/genetics , RNA, Messenger/genetics , RNA, Messenger/immunology , Transcriptome , Up-Regulation , Uterine Cervical Neoplasms/genetics
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