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TRPM2反义RNA通过miR-6764-5p上调附近基因TRPM2，促进卵巢癌细胞增殖并抑制细胞凋亡。

TRPM2-AS promotes ovarian cancer cell proliferation and inhibits cell apoptosis by upregulating the nearby gene TRPM2 via miR-6764-5p.

作者信息

Zhu Wei, Mao Shiqin, Jiang Juan

机构信息

Department of Gynecology, People's Hospital of Jingjiang, No. 28, Zhongzhou Road, Jingjiang City, Taizhou City, 214500, Jiangsu Province, China.

出版信息

Cell Div. 2024 Aug 27;19(1):26. doi: 10.1186/s13008-024-00130-0.

DOI:10.1186/s13008-024-00130-0
PMID:39192251
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11351637/
Abstract

Ovarian cancer (OC) becomes a fatal gynecologic malignant cancer in females worldwide. Target therapy is a promising therapeutical choice for patients with OC, and identifying biomarkers and exploring molecular mechanisms are necessary. In this study, the functions and mechanism of long noncoding RNA transient receptor potential cation channel subfamily M member 2 antisense RNA (TRPM2-AS) in OC were explored. TRPM2-AS expression in OC cells was analyzed utilizing reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8) and colony forming assays were carried out to explore the influence of TRPM2-AS on OC cell viability and proliferation. Cell apoptosis was detected using TdT-mediated dUTP Nick-End labeling (TUNEL) and flow cytometry analysis. Protein expression of apoptotic markers was subjected to western blotting. RNA pulldown or luciferase reporter assays were applied to explore the interaction between TRPM2-AS and miR-6764-5p or the binding of miR-6764-5p and TRPM2. The results showed that TRPM2-AS is highly expressed in OC cells and was mainly localized in cytoplasm. TRPM2-AS depletion suppressed OC cell viability and proliferation while increasing cell apoptotic rate. TRPM2 displayed a high level in OC cells and was positively regulated by TRPM2-AS. TRPM2-AS interacted with miR-6764-5p and thereby upregulated TRPM2 expression. In addition, TRPM2 overexpression reversed the repressive impact of TRPM2-AS depletion on malignant OC cellular process. In conclusion, TRPM2-AS promotes OC cell viability and proliferation while enhancing cell apoptosis through interaction with miR-6764-5p to regulate TRPM2 level.

摘要

卵巢癌（OC）是全球女性中一种致命的妇科恶性肿瘤。靶向治疗是OC患者一种有前景的治疗选择，识别生物标志物并探索分子机制很有必要。在本研究中，探讨了长链非编码RNA瞬时受体电位阳离子通道亚家族M成员2反义RNA（TRPM2-AS）在OC中的功能和机制。利用逆转录定量聚合酶链反应（RT-qPCR）分析OC细胞中TRPM2-AS的表达。进行细胞计数试剂盒-8（CCK-8）和集落形成试验，以探讨TRPM2-AS对OC细胞活力和增殖的影响。使用TdT介导的dUTP缺口末端标记（TUNEL）和流式细胞术分析检测细胞凋亡。对凋亡标志物的蛋白表达进行蛋白质印迹分析。应用RNA下拉或荧光素酶报告基因试验来探索TRPM2-AS与miR-6764-5p之间的相互作用或miR-6764-5p与TRPM2的结合。结果表明，TRPM2-AS在OC细胞中高表达，且主要定位于细胞质中。TRPM2-AS的缺失抑制了OC细胞的活力和增殖，同时增加了细胞凋亡率。TRPM2在OC细胞中呈现高水平，且受TRPM2-AS的正向调控。TRPM2-AS与miR-6764-5p相互作用，从而上调TRPM2的表达。此外，TRPM2的过表达逆转了TRPM2-AS缺失对恶性OC细胞进程的抑制作用。总之，TRPM2-AS通过与miR-6764-5p相互作用调节TRPM2水平，从而促进OC细胞的活力和增殖，同时增强细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/8ec336f75cf1/13008_2024_130_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/8ec336f75cf1/13008_2024_130_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/69c4d22baaf3/13008_2024_130_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/2571eafad3be/13008_2024_130_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/cf1cc8707089/13008_2024_130_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/fbc94f81ba6f/13008_2024_130_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5953/11351637/8ec336f75cf1/13008_2024_130_Fig6_HTML.jpg

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本文引用的文献

1
A macrophage related signature for predicting prognosis and drug sensitivity in ovarian cancer based on integrative machine learning.基于集成机器学习的巨噬细胞相关特征预测卵巢癌预后和药物敏感性。
BMC Med Genomics. 2023 Oct 2;16(1):230. doi: 10.1186/s12920-023-01671-z.
2
Identification of TRPM2 as a prognostic factor correlated with immune infiltration in ovarian cancer.鉴定 TRPM2 作为与卵巢癌免疫浸润相关的预后因素。
J Ovarian Res. 2023 Aug 22;16(1):169. doi: 10.1186/s13048-023-01225-y.
3
Identification of TRPM2 as a Potential Therapeutic Target Associated with Immune Infiltration: A Comprehensive Pan-Cancer Analysis and Experimental Verification in Ovarian Cancer.
鉴定TRPM2作为与免疫浸润相关的潜在治疗靶点：一项全面的泛癌分析及卵巢癌实验验证
Int J Mol Sci. 2023 Jul 25;24(15):11912. doi: 10.3390/ijms241511912.
4
Long noncoding RNA LOC646029 functions as a ceRNA to suppress ovarian cancer progression through the miR-627-3p/SPRED1 axis.长链非编码RNA LOC646029作为竞争性内源RNA，通过miR-627-3p/SPRED1轴抑制卵巢癌进展。
Front Med. 2023 Oct;17(5):924-938. doi: 10.1007/s11684-023-1004-z. Epub 2023 Jul 12.
5
lncRNA GAS5 suppression of the malignant phenotype of ovarian cancer via the miR-23a-WT1 axis.长链非编码RNA GAS5通过miR-23a-WT1轴抑制卵巢癌的恶性表型。
Ann Transl Med. 2023 Jan 31;11(2):119. doi: 10.21037/atm-22-6394.
6
Cancer statistics, 2023.癌症统计数据，2023 年。
CA Cancer J Clin. 2023 Jan;73(1):17-48. doi: 10.3322/caac.21763.
7
In silico Identification of Hypoxic Signature followed by reverse transcription-quantitative PCR Validation in Cancer Cell Lines.在癌症细胞系中通过反向转录定量 PCR 验证进行缺氧特征的计算机识别。
Iran Biomed J. 2023 Jan 1;27(1):23-33. doi: 10.52547/ibj.3803.
8
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9
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Mol Med. 2022 Sep 13;28(1):112. doi: 10.1186/s10020-022-00521-5.
10
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J Mol Histol. 2022 Aug;53(4):699-712. doi: 10.1007/s10735-022-10080-y. Epub 2022 Jul 6.