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(searched for: doi:10.4103/jcrt.jcrt_132_17)
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Yingli Zhang, Xiaoliang Shi, Jiejie Zhang, Xi Chen, Peng Zhang, Angen Liu,
Published: 11 January 2021
Scientific Reports, Volume 11, pp 1-10; https://doi.org/10.1038/s41598-020-79694-0

Abstract:
Ovarian cancer is one of the most common cancers in women and is often diagnosed as advanced stage because of the subtle symptoms of early ovarian cancer. To identify the somatic alterations and new biomarkers for the diagnosis and targeted therapy of Chinese ovarian cancer patients, a total of 65 Chinese ovarian cancer patients were enrolled for detection of genomic alterations. The most commonly mutated genes in ovarian cancers were TP53 (86.15%, 56/65), NF1 (13.85%, 9/65), NOTCH3 (10.77%, 7/65), and TERT (10.77%, 7/65). Statistical analysis showed that TP53 and LRP1B mutations were associated with the age of patients, KRAS, TP53, and PTEN mutations were significantly associated with tumor differentiation, and MED12, LRP2, PIK3R2, CCNE1, and LRP1B mutations were significantly associated with high tumor mutational burden. The mutation frequencies of LRP2 and NTRK3 in metastatic ovarian cancers were higher than those in primary tumors, but the difference was not significant (P = 0.072, for both). Molecular characteristics of three patients responding to olapanib supported that BRCA mutation and HRD related mutations is the target of olaparib in platinum sensitive patients. In conclusion we identified the somatic alterations and suggested a group of potential biomarkers for Chinese ovarian cancer patients. Our study provided a basis for further exploration of diagnosis and molecular targeted therapy for Chinese ovarian cancer patients.
Changhe Wang, Weimin Zhang, Shouli Xing, Zhaoxia Wang, Ju Wang, Jin Qu
Published: 1 October 2019
Anti-Cancer Drugs, Volume 30, pp 917-924; https://doi.org/10.1097/cad.0000000000000801

Abstract:
Previous studies have shown that microRNAs are involved in the pathogenesis of ovarian carcinoma (OC). However, the abnormal expression and function of miR-342-3p have not been reported in OC. Therefore, this research was designed to explore its role in OC. In this study, qRT-PCR assay showed that the expression level of miR-342-3p was reduced in OC tissues and cell lines. Functionally, Transwell assay suggested that overexpression of miR-342-3p suppressed cell migration and invasion in OC. In addition, forkhead box protein Q1 (FOXQ1) was confirmed to be a direct target gene by luciferase activity assay. Furthermore, FOXQ1 was found to be upregulated and function as an oncogene in OC. More importantly, miR-342-3p was negatively correlated with FOXQ1 expression in OC tissues. Furthermore, overexpression of FOXQ1 could partially rescue inhibitory effect of miR-342-3p on cell migration and invasion in OC. In brief, we concluded that miR-342-3p inhibited migration and invasion of OC cells through suppressing FOXQ1 expression.
Published: 25 September 2019
Abstract:
MiRNAs (miRNA) are small RNA molecules that are not to expressed to proteins. Their size is 20–22 nucleotides in length and they are highly conserved molecules among the species. miRNAs are synthesized in the nucleus as a primary miRNA. Primary miRNA is transferred to cytoplasm by Xpo5 protein (exportin-5) and then is processed by Dicer enzyme to a 22-nucleotide-sized long mature miRNA. miRNAs are differentially expressed in different diseases and are released into plasma by normal and tumor tissues during the cell metabolism. Ovarian carcinoma is the deadliest cancer among women. When the disease was diagnosed, the disease usually progressed. Currently, there is no biological marker to detect ovarian carcinoma at an early stage. Furthermore, there is a need for markers that are sensitive to chemotherapy changes and early detection of the disease. Because of this, miRNAs can be detected in plasma and can be used as highly significant biological markers and therapeutic targets for ovarian carcinoma. When the literature of the last 5 years is searched, there are many studies about miRNA and ovarian carcinoma. In this chapter, studies examining the relationship between ovarian carcinoma and miRNA from different angles are summarized under different sections.
Marta Brunetti, , Julie Staurseth, Ben Davidson, Sverre Heim,
Published: 4 June 2019
Journal: Oncotarget
Oncotarget, Volume 10, pp 3614-3624; https://doi.org/10.18632/oncotarget.26942

Abstract:
// Marta Brunetti1,2,*, Antonio Agostini1,*, Julie Staurseth1, Ben Davidson2,3, Sverre Heim1,3 and Francesca Micci1 1 Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway 2 Department of Pathology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway 3 Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway * These authors contributed equally to this work Correspondence to: Francesca Micci, email: [email protected] Keywords: uterine carcinosarcomas; ovarian carcinosarcomas; mutational analysis; gene expression; miRNA expression Received: March 06, 2019 Accepted: April 29, 2019 Published: June 04, 2019 ABSTRACT Gynaecological carcinosarcomas are rare biphasic tumours which are highly aggressive. We performed molecular investigations on a series of such tumours arising in the uterus (n = 16) and ovaries (n = 10) to gain more information on their mutational landscapes and the expression status of the genes HMGA1/2, FHIT, LIN28A, and MTA1, the pseudogenes HMGA1P6 and HMGA1P7, and the miRNAs known to influence expression of the above-mentioned genes. In uterine carcinosarcomas (UCS), we identified mutations in KRAS, PIK3CA, and TP53 with a frequency of 6%, 31%, and 75%, respectively, whereas in ovarian carcinosarcomas (OCS), TP53 was the only mutated gene found (30%). An inverse correlation was observed between overexpression of HMGA1/2, LIN28A, and MTA1 and downregulation of miRNAs such as let-7a, let-7d, miR26a, miR16, miR214, and miR30c in both UCS and OCS. HMGA2 was expressed in its full length in 14 UCS and 9 OCS; in the remaining tumours, it was expressed in its truncated form. Because FHIT was normally expressed while miR30c was downregulated, not both downregulated as is the case in several other carcinomas, alterations of the epithelial-mesenchymal transition through an as yet unknown mechanism seems to be a feature of carcinosarcomas.
Shihui Liu, Xiuxiu Li,
Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Volume 27, pp 165-171; https://doi.org/10.3727/096504018x15193506006164

Abstract:
MiR-30c has been acknowledged as a tumor suppressor in various human cancers, such as ovarian cancer, gastric cancer, and prostate cancer. However, the role of miR-30c in glioblastoma (GBM) needs to be investigated. In our study, we found that the expression of miR-30c was significantly downregulated in GBM tissues and cell lines. We found that overexpression of miR-30c inhibited cellular proliferation of GBM cells in vitro and in vivo. More GBM cells were arrested in the G0 phase after miR-30c overexpression. Moreover, we showed that miR-30c overexpression suppressed the migration and invasion of GBM cells. Mechanistically, we found that SOX9 was a direct target of miR-30c in GBM cells. Overexpression of miR-30c inhibited the mRNA and protein levels of SOX9 in GBM cells. Moreover, there was a negative correlation between the expression of miR-30c and SOX9 in GBM tissues. Finally, we showed that restoration of SOX9 in GBM cells reversed the proliferation, migration, and invasion of GBM cells transfected with miR-30c mimic. Collectively, our results demonstrated that miR-30c suppressed the proliferation, migration, and invasion of GBM cells via targeting SOX9.
Xin Chen, Ri-Xin Chen, Wen-Su Wei, Yong-Hong Li, Zi-Hao Feng, Lei Tan, Jie-Wei Chen, Gang-Jun Yuan, Si-Liang Chen, , et al.
Clinical Cancer Research, Volume 24, pp 6319-6330; https://doi.org/10.1158/1078-0432.ccr-18-1270

Abstract:
Purpose: Circular RNAs (circRNAs), a novel class of noncoding RNAs, have recently drawn lots of attention in the pathogenesis of human cancers. However, the role of circRNAs in cancer cells epithelial–mesenchymal transition (EMT) remains unclear. In this study, we aimed to identify novel circRNAs that regulate urothelial carcinoma of the bladder (UCB) cells’ EMT and explored their regulatory mechanisms and clinical significance in UCBs. Experimental Design: We first screened circRNA expression profiles using a circRNA microarray in paired UCB and normal tissues, and then studied the clinical significance of an upregulated circRNA, circPRMT5, in a large cohort of patients with UCB. We further investigated the functions and underlying mechanisms of circPRMT5 in UCB cells’ EMT. Moreover, we evaluated the regulation effect of circPRMT5 on miR-30c, and its target genes, SNAIL1 and E-cadherin, in two independent cohorts from our institute and The Cancer Genome Atlas (TCGA). Results: We demonstrated that upregulated expression of circPRMT5 was positively associated with advanced clinical stage and worse survival in patients with UCB. We further revealed that circPRMT5 promoted UCB cell's EMT via sponging miR-30c. Clinical analysis from two independent UCB cohorts showed that the circPRMT5/miR-30c/SNAIL1/E-cadherin pathway was essential in supporting UCB progression. Importantly, we identified that circPRMT5 was upregulated in serum and urine exosomes from patients with UCB, and significantly correlated with tumor metastasis. Conclusions: CircPRMT5 exerts critical roles in promoting UCB cells’ EMT and/or aggressiveness and is a prognostic biomarker of the disease, suggesting that circPRMT5 may serve as an exploitable therapeutic target for patients with UCB.
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