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SPOCK2 通过调控 Wnt/-Catenin 信号通路促进卵巢癌的恶性行为。

SPOCK2 Promotes the Malignant Behavior of Ovarian Cancer via Regulation of the Wnt/-Catenin Signaling Pathway.

机构信息

Obstetrical Department, Taian City Central Hospital, Taian, China.

Ultrasonic Diagnosis and Treatment Center, Taian City Central Hospital, Taian, China.

出版信息

Biomed Res Int. 2022 Sep 23;2022:9223954. doi: 10.1155/2022/9223954. eCollection 2022.

DOI:10.1155/2022/9223954
PMID:36193300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9525767/
Abstract

BACKGROUND

Ovarian cancer (OC) is a common clinical gynecological disease, which seriously threatens women's health and life. We investigated the roles of SPOCK2 in OC and its associated molecular mechanism in the current study.

METHODS

The expressions and prognostic value of SPOCK2 in OC were identified using the clinical data and data from the GEPIA database. Then, SPOCK2 silence was implemented to search functions of SPOCK2 in OC cells. CCK-8 was used to examine cell proliferation. Cell apoptosis was detected by flow cytometry. The OC cell invasion and migration were evaluated by transwell assays.

RESULTS

Overexpressed SPOCK2 was identified in OC, which was correlated with poor prognosis and a shorter survival rate. SPOCK2 downregulation significantly suppressed OC cell proliferation, migration, and invasion, and cell apoptosis was markedly promoted by SPOCK2 silence. Meanwhile, SPOCK2 knockdown could effectively suppress Wnt/-catenin.

CONCLUSION

SPOCK2 exerted crucial functions in OC progression and could serve as a promising candidate for OC targeted therapy.

摘要

背景

卵巢癌（OC）是一种常见的临床妇科疾病，严重威胁着妇女的健康和生命。本研究旨在探讨 SPOCK2 在 OC 中的作用及其相关的分子机制。

方法

本研究通过临床数据和 GEPIA 数据库中的数据，确定 SPOCK2 在 OC 中的表达和预后价值。然后，通过沉默 SPOCK2 来研究 SPOCK2 在 OC 细胞中的功能。通过 CCK-8 检测细胞增殖。通过流式细胞术检测细胞凋亡。通过 Transwell 实验评估 OC 细胞的侵袭和迁移。

结果

在 OC 中发现 SPOCK2 过表达，与不良预后和生存率降低相关。沉默 SPOCK2 可显著抑制 OC 细胞的增殖、迁移和侵袭，促进细胞凋亡。同时，SPOCK2 敲低可有效抑制 Wnt/-catenin。

结论

SPOCK2 在 OC 进展中发挥重要作用，可作为 OC 靶向治疗的有前途的候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/138889bb41ee/BMRI2022-9223954.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/016b61385bdd/BMRI2022-9223954.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/41bb264f65bf/BMRI2022-9223954.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/cf34158812c9/BMRI2022-9223954.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/b224f43b4dd4/BMRI2022-9223954.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/4a8ab1df8614/BMRI2022-9223954.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/138889bb41ee/BMRI2022-9223954.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/016b61385bdd/BMRI2022-9223954.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/41bb264f65bf/BMRI2022-9223954.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/acf16dff64d4/BMRI2022-9223954.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/cf34158812c9/BMRI2022-9223954.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/b224f43b4dd4/BMRI2022-9223954.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/4a8ab1df8614/BMRI2022-9223954.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e12/9525767/138889bb41ee/BMRI2022-9223954.007.jpg

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