Phosphoproteomic response mapping to anti-angiogenic agents bevacizumab and cediranib in high-grade serous ovarian and endometrial cancer cell lines

2021 ◽  
Vol 162 ◽  
pp. S235-S236
Author(s):  
Stephanie Leiva ◽  
Andreea Newtson ◽  
Jianling Bi ◽  
Eric Devor ◽  
Yuping Zhang ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
High Grade ◽  
Endometrial Cancer Cell ◽  
Response Mapping

scholarly journals The Effects on Ishikawa Endometrial Cancer Cell Lines upon Treatment with Hormonal Agents and Novel Drug Target

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Pooja Pandita ◽  
Xiyin Wang ◽  
Shannon Hawkins
Keyword(s):  
Endometrial Cancer ◽  
Steroid Hormones ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cellular Proliferation ◽  
Steroid Hormone ◽  
Endometrial Adenocarcinoma ◽  
Cancer Cell Lines ◽  
High Grade ◽  
Endometrial Cancer Cell

Background and Hypothesis: Endometrial cancer is the most common gynecological malignancy in the US and will claim the lives of over 12,000 women in 2019. Women with high-risk histologic tumors, such as high-grade endometrial adenocarcinoma, represent over 50% of these deaths. Novel treatments are needed to treat these aggressive tumors. Decreased expression of the ribonuclease DICER is associated with high-grade and recurrent endometrial adenocarcinoma. To study the role of DICER in endometrial cancer, we used CRISPR/Cas9 to delete DICER in an endometrial cancer cell line. RNA sequencing revealed dysregulation of steroid hormone receptor signaling and high expression of APEX1 [apurinic/apyrimidinic endonuclease 1 (Ref-1/APE1)]. Elevated levels of Ref-1/APE1 have been found in various tumor types, and Ref1/APE1 inhibitors are in clinical trials. We hypothesize that our DICER deleted cell lines will be hormone insensitive yet respond to Ref-1/APE1 inhibitors by decreasing cellular proliferation. Project Methods: Ingenuity Pathway Analysis provided an unbiased approach to determine dysregulated genes in steroid hormone signaling in our RNA transcriptomic data. QPCR was used to confirm gene expression in independent samples. Cells were treated with steroid hormones or Ref-1/APE1 inhibitors and proliferation was assessed using MTS. Results: DICER deleted cell lines had downregulated expression of steroid hormone receptors. Treatment with steroid hormones did not have a significant effect on proliferation. However, treatment with Ref-1/APE1 inhibitors resulted in a significant decrease in proliferation. Conclusion and Potential Impact: Ref-1/APE1 inhibitors affect cellular proliferation of endometrial cancer cell lines. Because survival has actually worsened for women with endometrial cancer, novel therapies such as Ref1/APE1 inhibitors deserve future study.

Mutations in tumor suppressor gene, FBXW7, are associated with carboplatin resistance in endometrial cancer cell lines

2015 ◽  
Vol 139 (1) ◽  
pp. 194 ◽  
Author(s):  
Alexandre Buckley de Meritens ◽  
Ayesha Joshi ◽  
Christopher Miller ◽  
Lora Hedrick Ellenson ◽  
Divya Gupta
Keyword(s):  
Endometrial Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Suppressor Gene ◽  
Endometrial Cancer Cell

Variances in the Expression Profile of the EMT-Related Genes in Endometrial Cancer Lines In Vitro Study

2021 ◽  
Vol 22 ◽  
Author(s):  
Robert Nowakowski ◽  
Beniamin Grabarek ◽  
Anna Burnat-Olech ◽  
Dariusz Boroń ◽  
Monika Paul-Samojedny
Keyword(s):  
Endometrial Cancer ◽  
Expression Pattern ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cultures ◽  
Expression Profile ◽  
Histological Grade ◽  
Cancer Cell Lines ◽  
Endometrial Cancer Cell

Background: This study aimed to evaluate the variances in the expression pattern of mRNAs and miRNAs related to the EMT in the Ishikawa (histological grade 1; G1), EC-1A (histological grade 2; G2), and KLE (histological grade 3; G3) cell cultures under cisplatin treatment. Methods: Endometrial cancer cell lines were exposed to 75.22 mg (an average concentration of the drug used in patients with endometrial cancer) for 12.24 and 48 hours compared to the untreated cells (control). The molecular analysis included extraction of total RNA, microarray analysis (mRNA and miRNA), RTqPCR, and the ELISA assay. Results: Out of 226 mRNAs associated with the EMT, the number of mRNAs differentially expressed in endometrial cancer cell cultures treated with cisplatin compared to a control culture was as follows: Ishikawa line - 87 mRNAs; EC-1A - 84 mRNAs; KLE - 71 mRNAs (p<0.05). The greatest changes in the Ishikawa line treated with the drug compared to the control were noticed for mRNA STAT1 TGFβ1, SMAD3, FOXO8, whereas in EC-1A, they were mRNA TGFβ1, BAMBI, SMAD4, and in KLE mRNA COL1A1, FOXO8, TGFβ1. The analysis also showed that miR-106a, miR-30d, miR-300 are common for all cell lines used in this experiment. Conclusion: Cisplatin changes the expression profile of genes associated with EMT in endometrial cancer cell lines. It seems that the expression pattern of TGFβ1 might be a promising, supplementary molecular marker of the effectiveness of cisplatin therapy. The analysis showed that miR-30d, miR-300, and miR-106a are involved in the regulation of the expression of EMT-related genes.

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