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雌激素通过激活瞬时受体电位通道 C3 增强卵巢癌细胞的增殖和迁移。

Estrogen enhances the proliferation and migration of ovarian cancer cells by activating transient receptor potential channel C3.

机构信息

Department of Gynecology and Obstetrics, Xijing Hospital, Air Force Medical University, Xi'an, 710032, Shannxi, China.

Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, 710054, Shaanxi, China.

出版信息

J Ovarian Res. 2020 Feb 22;13(1):20. doi: 10.1186/s13048-020-00621-y.

DOI:10.1186/s13048-020-00621-y
PMID:32087757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7035653/
Abstract

BACKGROUND

Recent studies have suggested that estrogen (E2) plays an important role in epithelial ovarian cancer (EOC). However, the mechanism of E2 in ovarian cancers is unclear. The purpose of this study was to investigate the effect of E2 on ovarian cancers and illuminate the mechanism of E2 in promote ovarian cancers proliferation.

RESULTS

We demonstrated that E2 stimulated the proliferation and invasion of ovarian cancer cells. In this study, ovarian cancer specimens were also analyzed for transient receptor potential channel C3 (TRPC3) expression; TRPC3 expression levels were higher in ovarian cancer samples than in normal ovarian tissue samples. Previous studies have shown that TRPC3 contributes to the progression of human ovarian cancer. In this study, we further investigated the interaction between E2 and TRPC3. We found that E2 stimulation enhanced the expression of TRPC3 at both the mRNA and protein levels. E2 stimulation enhanced the influx of Ca2. Moreover, siRNA-mediated silencing of TRPC3 expression inhibited the ability of E2 to stimulate the influx of Ca2.

CONCLUSIONS

In conclusion, TRPC3 plays a significant role in the stimulatory activity of E2 and could be a therapeutic target for the treatment of EOC. Furthermore, this study elucidates the molecular mechanism by which E2 promotes the proliferation and migration of EOC cells.

摘要

背景

最近的研究表明，雌激素（E2）在卵巢上皮性癌（EOC）中发挥着重要作用。然而，E2 在卵巢癌中的作用机制尚不清楚。本研究旨在探讨 E2 对卵巢癌的影响，并阐明 E2 促进卵巢癌增殖的机制。

结果

我们证实 E2 可刺激卵巢癌细胞的增殖和侵袭。在这项研究中，还分析了卵巢癌标本中瞬时受体电位通道 C3（TRPC3）的表达；卵巢癌样本中的 TRPC3 表达水平高于正常卵巢组织样本。先前的研究表明 TRPC3 有助于人类卵巢癌的进展。在这项研究中，我们进一步研究了 E2 和 TRPC3 之间的相互作用。我们发现 E2 刺激可增强 TRPC3 在 mRNA 和蛋白质水平的表达。E2 刺激可增强 Ca2+内流。此外，siRNA 介导的 TRPC3 表达沉默抑制了 E2 刺激 Ca2+内流的能力。

结论

综上所述，TRPC3 在 E2 的刺激活性中起重要作用，可能成为治疗 EOC 的治疗靶点。此外，本研究阐明了 E2 促进 EOC 细胞增殖和迁移的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/4d6e362fae22/13048_2020_621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/c346fc07d82d/13048_2020_621_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/4d02dba433e3/13048_2020_621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/64350cc821b9/13048_2020_621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/714befb4bcd9/13048_2020_621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/4d6e362fae22/13048_2020_621_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/c346fc07d82d/13048_2020_621_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/4d02dba433e3/13048_2020_621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/64350cc821b9/13048_2020_621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/714befb4bcd9/13048_2020_621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0287/7035653/4d6e362fae22/13048_2020_621_Fig5_HTML.jpg

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本文引用的文献

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