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LncSOX4 在卵巢上皮性癌的发生发展中发挥致癌作用,促进细胞增殖,抑制细胞凋亡。

LncSOX4 serves an oncogenic role in the tumorigenesis of epithelial ovarian cancer by promoting cell proliferation and inhibiting apoptosis.

机构信息

Gynecology Department, Hubei Women and Children's Hospital, Wuhan, Hubei 430070, P.R. China.

Urology Department, Hubei Cancer Hospital, Wuhan, Hubei 430079, P.R. China.

出版信息

Mol Med Rep. 2018 Jun;17(6):8282-8288. doi: 10.3892/mmr.2018.8892. Epub 2018 Apr 18.

DOI:10.3892/mmr.2018.8892
PMID:29693704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5984009/
Abstract

Epithelial ovarian cancer is one of the primary causes of gynecological cancer mortality. Increasing evidence has suggested that long non‑coding RNAs (lncRNAs) may serve a pivotal role in cancer development. To determine whether Lnc SRY‑box 4 (SOX4), an lncRNA, promotes the self‑renewal of liver tumor cells and contributes to the development of epithelial ovarian cancer, the present study investigated the expression of LncSOX4 in clinical epithelial ovarian cancer tissues and non‑cancer controls by reverse transcription‑quantitative polymerase chain reaction analysis. In addition, siRNA targeting LncSOX4 was designed and transfected into epithelial ovarian cancer cells to further assess the effect of knocking out LncSOX4 on cellular apoptosis, cell viability, proliferation and the cell cycle. The results demonstrated that the LncSOX4 expression level was significantly upregulated in epithelial ovarian cancer tissues (3.98 vs. 1.71, P<0.001). Silencing LncSOX4 in the SKOV3 and OVCAR3 cell lines significantly impaired cell proliferation (P<0.001). Cell cycle assays revealed that the proportion of cells in the G0/G1 phase increased significantly, whereas those in the S phase and G2/M phase decreased. Apoptosis rate additionally increased following knockdown of LncSOX4 in the two cell lines. Furthermore, it was observed that an increased LncSOX4 expression level was positively associated with larger tumor sizes, more advanced tumor grade and more distant metastases.

摘要

上皮性卵巢癌是妇科癌症死亡的主要原因之一。越来越多的证据表明,长链非编码 RNA(lncRNA)可能在癌症发展中发挥关键作用。为了确定 lncRNA SOX4 盒 4(SOX4)是否促进肝癌细胞的自我更新并有助于上皮性卵巢癌的发展,本研究通过逆转录-定量聚合酶链反应分析,检测了临床上皮性卵巢癌组织和非癌对照中 LncSOX4 的表达。此外,设计了靶向 LncSOX4 的 siRNA 并转染上皮性卵巢癌细胞,以进一步评估敲除 LncSOX4 对细胞凋亡、细胞活力、增殖和细胞周期的影响。结果表明,上皮性卵巢癌组织中 LncSOX4 的表达水平显著上调(3.98 比 1.71,P<0.001)。沉默 SKOV3 和 OVCAR3 细胞系中的 LncSOX4 显著抑制细胞增殖(P<0.001)。细胞周期分析显示,G0/G1 期细胞比例显著增加,而 S 期和 G2/M 期细胞比例减少。敲低两种细胞系中的 LncSOX4 后,细胞凋亡率也增加。此外,观察到 LncSOX4 表达水平的增加与肿瘤体积增大、肿瘤分级更高级和远处转移更多呈正相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/a635b519ce77/MMR-17-06-8282-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/35b06c3bacdb/MMR-17-06-8282-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/6ef2ccdb33d5/MMR-17-06-8282-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/c1e3f2246663/MMR-17-06-8282-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/4f317aeb722d/MMR-17-06-8282-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/520691ec7f76/MMR-17-06-8282-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/a635b519ce77/MMR-17-06-8282-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/35b06c3bacdb/MMR-17-06-8282-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/6ef2ccdb33d5/MMR-17-06-8282-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/c1e3f2246663/MMR-17-06-8282-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/4f317aeb722d/MMR-17-06-8282-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/520691ec7f76/MMR-17-06-8282-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb08/5984009/a635b519ce77/MMR-17-06-8282-g05.jpg

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