Metformin interrupts bidirectional signaling between tumor and mesothelial cells by blocking OvCa cell TGF-β signaling and mesothelial cell production of CCL2 and IL-8.
Metformin interrupts bidirectional signaling between tumor and mesothelial cells by blocking OvCa cell TGF-β signaling and mesothelial cell production of CCL2 and IL-8.
Expression of the Immune Checkpoints LAG-3 and PD-L1 in High-grade Serous Ovarian Carcinoma: Relationship to Tumor-associated Lymphocytes and Germline BRCA Status.
Expression of the Immune Checkpoints LAG-3 and PD-L1 in High-grade Serous Ovarian Carcinoma: Relationship to Tumor-associated Lymphocytes and Germline BRCA Status.
Circular RNA itchy E3 ubiquitin protein ligase (circ-ITCH), a novel circular RNA originated from several exons of ITCH and located on chromosome 20q11.22, was proved to be declined in many malignant tumors, such as melanoma and ovarian cancer, resulting in tumor occurrence and progression.
It was revealed via an in vivo study that miR-139 remarkably inhibited the growth of malignancies by downregulating ATP7A in nude mice. miR-139 represses the development of malignancies in OC by directly targeting ATP7A, offering an innovative approach for molecular therapy of OC.
We used CRISPR-DS to deeply sequence (mean Duplex depth ~3000×) the TP53 gene in 30 Pap tests from 21 women without cancer and 9 women with serous ovarian carcinoma with known TP53 driver mutations.
Taken together, LncRNA-ROR promoted EMT by the miR-145/FLNB regulatory axis in ovarian cancer, providing a potential therapeutic target for ovarian cancer.
In addition, knockdown of INHBA in cancer cells impaired cancer xenograft growth through reducing OC stromal fibroblast activation <i>in vivo.</i> Further results confirmed that Smad2 signaling pathway was involved in INHBA-induced stromal fibroblast activation, and inhibiting this pathway could effectively reverse activation of stromal fibroblasts.
Using cell lines representative of P53 wild-type ovarian cancer (A2780), and P53 mutant ovarian cancer (SKOV3), cells were implanted in the flank of athymic nude female mice.
In conclusion, SRO-91 analog effects on tumor dissemination and its safety regarding non-cancerous (normal) cells are encouraging findings a promising drug for the treatment of ovarian cancer.
These findings suggest that novel missense variants within the helicase domain of BRIP1 may confer risk for both breast and ovarian cancer and highlight the importance of functional testing for additional variants.