Long Non-Coding RNA X Inactive Specific Transcript Suppressed the Proliferation and Invasion of Ovarian Cancer Cells by Restricting the Expression of Staphylococcal Nuclease Domain Containing 1

2020 ◽  
Vol 10 (12) ◽  
pp. 1793-1799
Author(s):  
Shenglan Chen ◽  
Ai Jiang ◽  
Yan Wang ◽  
Yina Wang

Ovarian cancer is one kind of a deadly gynecological malignancy. Recent study has shown that SND1 was associated with the development of ovarian cancer. Furthermore, the expression of lncRNA XIST in ovarian cancer was down-regulated. However, it is unclear whether lncRNA XIST could affect the occurrence and development of ovarian cancer by targeting SND1. In this study, we used the lentivirus to establish the overexpression and knockdown SND1 ovarian cancer cells. And we next detected the proliferation and invasion of these cells in diverse groups. Then, the luciferase assays were performed to detect the targeted effect of lncRNA XIST on SND1 and determined the expression of SND1 in the overexpressed lncRNA XIST ovarian cancer cells. We found that SND1 promoted the proliferation and invasion of ovarian cancer cells. And the lncRNA XIST targeted and suppressed the expression of SND1. Overexpression of lncRNA XIST inhibited the proliferation and invasion of ovarian cancer cells. However, the overexpression of SND1 alleviated the inhibitory efficacy of lncRNA XIST on the proliferation and invasion of ovarian cancer cells. LncRNA XIST inhibited the proliferation and invasion of ovarian cancer by suppressing the expression of SND1.

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qingjuan Meng ◽  
Ningning Wang ◽  
Guanglan Duan

Abstract Background X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. Methods RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. Results The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. Conclusion XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.


Neoplasma ◽  
2015 ◽  
Vol 62 (03) ◽  
pp. 432-438 ◽  
Author(s):  
F. WANG ◽  
J. ZHOU ◽  
X. XIE ◽  
J. HU ◽  
L. CHEN ◽  
...  

2020 ◽  
Vol 52 (3) ◽  
pp. 798-814 ◽  
Author(s):  
De-Ying Wang ◽  
Na Li ◽  
Yu-Lan Cui

PurposeColon cancer-associated transcript 1 (CCAT1) was identified as an oncogenic long non-coding RNA (lncRNA) in a variety of cancers. However, there was a lack of understanding of the mechanism by which CCAT1 conferred cisplatin (also known as DDP) resistance in ovarian cancer cells.Materials and MethodsCell viability of A2780, SKOV3, A2780/DDP, and SKOV3/DDP cells upon cisplatin treatment was monitored by MTT assay. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) detected the expression levels of CCAT1 and miR-454. The effect of sh-CCAT1 on cisplatin response was investigated in xenografts study. Bioinformatic analysis, luciferase reporter assay and qRT-PCR were conducted to validate the direct interaction among CCAT1, miR-454, and survivin. Apoptosis was determined by flow cytometry after dual staining of Annexin-V-FITC/propidium iodide, and the expression of apoptosis-related proteins Bcl-2, Bax and survivin were detected by qRT-PCR and Western blotting. Xenograft study was conducted to monitor <i>in vivo</i> tumor formation.ResultsCCAT1 was highly expressed in cisplatin-resistant ovarian cancer cell line A2780/DDP and SKOV3/DDP. Knockdown of CCAT1 restored sensitivity to cisplatin <i>in vitro</i> and <i>in vivo</i>. Our data revealed that silencing of CCAT1 promoted cisplatin-induced apoptosis via modulating the expression of pro- or anti-apoptotic proteins Bax, Bcl-2, and survivin. CCAT1 directly interacted with miR-454, and miR-454 overexpression potentiated cisplatin-induced apoptosis. Survivin was identified as a functional target of miR-454, restoration of survivin attenuated the effect of miR-454 on cisplatin response. In addition, miR-454 inhibitor or overexpression of survivin was found to abolish sh-CCAT1–induced apoptosis upon cisplatin treatment.ConclusionCCAT1/miR-454/survivin axis conferred cisplatin resistance in ovarian cancer cells.


2018 ◽  
Vol 35 (3) ◽  
pp. 247-266 ◽  
Author(s):  
Elahe Seyed Hosseini ◽  
Marziyeh Alizadeh Zarei ◽  
Sadegh Babashah ◽  
Roohollah Nakhaei Sistani ◽  
Majid Sadeghizadeh ◽  
...  

2018 ◽  
Vol 109 (7) ◽  
pp. 2188-2198 ◽  
Author(s):  
Yangcheng Liu ◽  
Yong Wang ◽  
Xinming Fu ◽  
Zhi Lu

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