scholarly journals Ovarian Cancer Metastasis: A Unique Mechanism of Dissemination

10.5772/64700 ◽  
2016 ◽  
Author(s):  
Anirban K. Mitra
Keyword(s):  
Ovarian Cancer ◽  
Cancer Metastasis ◽  
Unique Mechanism

scholarly journals LncRNA SPOCD1-AS from ovarian cancer extracellular vesicles remodels mesothelial cells to promote peritoneal metastasis via interacting with G3BP1

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Conghui Wang ◽  
Jiaying Wang ◽  
Xiameng Shen ◽  
Mingyue Li ◽  
Yongfang Yue ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Extracellular Vesicles ◽  
Peritoneal Metastasis ◽  
Cancer Metastasis ◽  
Cancer Therapeutics ◽  
Mesothelial Cells ◽  
Ovarian Cancer Cells ◽  
Adhesion Assay ◽  
Mesenchymal Transition

Abstract Background Metastasis is the key cause of death in ovarian cancer patients. To figure out the biological nature of cancer metastasis is essential for developing effective targeted therapy. Here we investigate how long non-coding RNA (lncRNA) SPOCD1-AS from ovarian cancer extracellular vesicles (EVs) remodel mesothelial cells through a mesothelial-to-mesenchymal transition (MMT) manner and facilitate peritoneal metastasis. Methods EVs purified from ovarian cancer cells and ascites of patients were applied to mesothelial cells. The MMT process of mesothelial cells was assessed by morphology observation, western blot analysis, migration assay and adhesion assay. Altered lncRNAs of EV-treated mesothelial cells were screened by RNA sequencing and identified by qRT-PCR. SPOCD1-AS was overexpressed or silenced by overexpression lentivirus or shRNA, respectively. RNA pull-down and RNA immunoprecipitation assays were conducted to reveal the mechanism by which SPOCD1-AS remodeled mesothelial cells. Interfering peptides were synthesized and applied. Ovarian cancer orthotopic implantation mouse model was established in vivo. Results We found that ovarian cancer-secreted EVs could be taken into recipient mesothelial cells, induce the MMT phenotype and enhance cancer cell adhesion to mesothelial cells. Furthermore, SPOCD1-AS embedded in ovarian cancer-secreted EVs was transmitted to mesothelial cells to induce the MMT process and facilitate peritoneal colonization in vitro and in vivo. SPOCD1-AS induced the MMT process of mesothelial cells via interacting with G3BP1 protein. Additionally, G3BP1 interfering peptide based on the F380/F382 residues was able to block SPOCD1-AS/G3BP1 interaction, inhibit the MMT phenotype of mesothelial cells, and diminish peritoneal metastasis in vivo. Conclusions Our findings elucidate the mechanism associated with EVs and their cargos in ovarian cancer peritoneal metastasis and may provide a potential approach for metastatic ovarian cancer therapeutics.

scholarly journals CD133 Promotes Adhesion to the Ovarian Cancer Metastatic Niche

2018 ◽  
Vol 11 ◽  
pp. 117906441876788 ◽  
Author(s):  
Lynn Roy ◽  
Alexander Bobbs ◽  
Rachel Sattler ◽  
Jeffrey L Kurkewich ◽  
Paige B Dausinas ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Metastasis ◽  
Ex Vivo ◽  
Surface Protein ◽  
Ovarian Cancer Cells ◽  
Metastatic Niche ◽  
Attractive Therapeutic Target ◽  
Peritoneal Mesothelium

Cancer stem cells (CSCs) are an attractive therapeutic target due to their predicted role in both metastasis and chemoresistance. One of the most commonly agreed on markers for ovarian CSCs is the cell surface protein CD133. CD133+ ovarian CSCs have increased tumorigenicity, resistance to chemotherapy, and increased metastasis. Therefore, we were interested in defining how CD133 is regulated and whether it has a role in tumor metastasis. Previously we found that overexpression of the transcription factor, ARID3B, increased the expression of PROM1 (CD133 gene) in ovarian cancer cells in vitro and in xenograft tumors. We report that ARID3B directly regulates PROM1 expression. Importantly, in a xenograft mouse model of ovarian cancer, knockdown of PROM1 in cells expressing exogenous ARID3B resulted in increased survival time compared with cells expressing ARID3B and a control short hairpin RNA. This indicated that ARID3B regulation of PROM1 is critical for tumor growth. Moreover, we hypothesized that CD133 may affect metastatic spread. Given that the peritoneal mesothelium is a major site of ovarian cancer metastasis, we explored the role of PROM1 in mesothelial attachment. PROM1 expression increased adhesion to mesothelium in vitro and ex vivo. Collectively, our work demonstrates that ARID3B regulates PROM1 adhesion to the ovarian cancer metastatic niche.

Abstract 2461: SIRT1 regulates ovarian cancer metastasis via altering the exosome release and glycogen deposition

2021 ◽  
Author(s):  
Sraddhya Roy ◽  
Ananya Das ◽  
Manisha Vernekar ◽  
Subhadip Das ◽  
Nabanita Chatterjee
Keyword(s):  
Ovarian Cancer ◽  
Cancer Metastasis ◽  
Glycogen Deposition

Superoxide Dismutase 2 is Necessary for Key Steps in the Transcoelomic Route of Ovarian Cancer Metastasis

2013 ◽  
Vol 65 ◽  
pp. S20
Author(s):  
Madhubhani LP Hemachandra ◽  
Usawadee Dier ◽  
Larissa M Uusitalo ◽  
Donghui Shin ◽  
Sarah a Engelberth ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Superoxide Dismutase ◽  
Cancer Metastasis ◽  
Key Steps ◽  
Superoxide Dismutase 2

scholarly journals Mucinous ovarian cancer metastasis to cervix: a rare case report

2021 ◽  
Author(s):  
Gatot Purwoto ◽  
Raditya Perdhana ◽  
Tantri Hellyanti ◽  
Trifonia Pingkan Siregar ◽  
Siti Rafiqah Fajri
Keyword(s):  
Ovarian Cancer ◽  
Case Report ◽  
Rare Case ◽  
Cancer Metastasis ◽  
Rare Case Report

scholarly journals AMPK-independent LKB1 activity is required for efficient epithelial ovarian cancer metastasis

2019 ◽  
Author(s):  
Adrian Buensuceso ◽  
Yudith Ramos Valdes ◽  
Gabriel E. DiMattia ◽  
Trevor G. Shepherd
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cell Survival ◽  
Cell Lines ◽  
Cancer Metastasis ◽  
Metastatic Potential ◽  
Metastatic Tumour ◽  
Ampk Signaling ◽  
Dual Specificity ◽  
Liver Kinase B1

ABSTRACTEpithelial ovarian cancer (EOC) spreads by direct dissemination of malignant cells and multicellular clusters, known as spheroids, into the peritoneum followed by implantation and growth on abdominal surfaces. Using a spheroid model system of EOC metastasis, we discovered that Liver kinase B1 (LKB1), encoded by theSTK11gene, and its canonical substrate AMP-activated protein kinase (AMPK) are activated in EOC spheroids, yet only LKB1 is required for cell survival. We have now generatedSTK11-knockout cell lines using normal human FT190 cells and three EOC cell lines, OVCAR8, HeyA8, and iOvCa147.STK11KO did not affect growth and viability in adherent culture, but it decreased anchorage-independent growth of EOC cells. EOC spheroids lacking LKB1 had markedly impaired growth and viability, whereas there was no difference in normal FT190 spheroids. To test whether LKB1 loss affects EOC metastasis, we performed intraperitoneal injections of OVCAR8-, HeyA8-, and iOvCa147-STK11KO cells, and respective controls. LKB1 loss exhibited a dramatic reduction on tumour burden and metastatic potential; in particular, OVCAR8-STK11KO tumours had evidence of extensive necrosis, apoptosis and hypoxia. Interestingly, LKB1 loss did not affect AMPKα phosphorylation in EOC spheroids and tumour xenografts, indicating that LKB1 signaling to support EOC cell survival in spheroids and metastatic tumour growth occurs via other downstream mediators. We identified the dual-specificity phosphatase DUSP4 as a commonly upregulated protein due to LKB1 loss; indeed,DUSP4knockdown in HeyA8-STK11KO cells restored spheroid formation and viability. Our results strongly indicate that intact LKB1 activity independent of downstream AMPK signaling is required during EOC metastasis.

The Tumor Microenvironment Takes Center Stage in Ovarian Cancer Metastasis

2018 ◽  
Vol 4 (8) ◽  
pp. 517-519 ◽  
Author(s):  
Marion Curtis ◽  
Abir Mukherjee ◽  
Ernst Lengyel
Keyword(s):  
Ovarian Cancer ◽  
Tumor Microenvironment ◽  
Cancer Metastasis ◽  
Center Stage
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