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人参皂苷 Rd 通过 H19/miR-675-5p/CDH1 轴抑制舌癌细胞的迁移和侵袭。

Ginsenoside Rd inhibits migration and invasion of tongue cancer cells through H19/miR-675-5p/CDH1 axis.

机构信息

Jilin University, Hospital of Stomatology, Department of Oral and Maxillofacial Surgery, Changchun, China.

Jilin University, College of Animal Science, Laboratory Animal Center, Changchun, China.

出版信息

J Appl Oral Sci. 2022 Sep 2;30:e20220144. doi: 10.1590/1678-7757-2022-0144. eCollection 2022.

DOI:10.1590/1678-7757-2022-0144
PMID:36074434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9444189/
Abstract

OBJECTIVE

Tongue squamous cell carcinoma (TSCC) is an oral cancer, with high malignancy and frequent early migration and invasion. Only a few drugs can treat tongue cancer. Ginsenoside Rd is a ginseng extract with anti-cancer effects. Many noncoding RNAs are abnormally expressed in tongue cancer, thus influencing its occurrence and development. H19 and miR-675-5p can promote cancer cell growth. This study aimed to analyze the regulation effect of ginsenoside Rd on H19 and miR-675-5p in tongue cancer.

METHODOLOGY

We used CCK8 and flow cytometry to study the growth and apoptosis. Transwell assay was used to assess invasion; wound-healing assay to assess migration; and colony formation assays to test the ability of cells to form colonies. H19, miR-675-5p, and CDH1 expressions were analyzed by qPCR. E-cadherin expression was detected using western blot. CRISPR/cas9 system was used for CDH1 knockout.

RESULTS

Ginsenoside Rd inhibited the growth and increased the apoptosis of SCC9 cells. Ginsenoside Rd also inhibited the migration and invasion of SCC9 cells. H19 and miR-675-5p were highly expressed, while CDH1 and E-cadherin expressions were low. H19 and miR-675-5p promoted SCC9 metastasis. In contrast, CDH1 and E-cadherin inhibited the metastasis of SCC9 cells. Bioinformatics analysis showed that miR-675-5p was associated with CDH1. H19 and miR-675-5p expressions decreased after ginsenoside Rd treatment, while CDH1 and E-cadherin expressions increased.

CONCLUSIONS

Ginsenoside Rd inhibits tongue cancer cell migration and invasion via the H19/miR-675-5p/CDH1 axis.

摘要

目的

舌鳞状细胞癌(TSCC)是一种口腔癌,具有高度恶性和频繁的早期迁移和侵袭。只有少数药物可以治疗舌癌。人参皂苷 Rd 是一种具有抗癌作用的人参提取物。许多非编码 RNA 在舌癌中异常表达,从而影响其发生和发展。H19 和 miR-675-5p 可以促进癌细胞生长。本研究旨在分析人参皂苷 Rd 对舌癌细胞中 H19 和 miR-675-5p 的调节作用。

方法

我们使用 CCK8 和流式细胞术研究细胞生长和凋亡。Transwell 测定法用于评估侵袭;划痕愈合试验用于评估迁移;集落形成试验用于测试细胞形成集落的能力。通过 qPCR 分析 H19、miR-675-5p 和 CDH1 的表达。通过 Western blot 检测 E-cadherin 的表达。CRISPR/cas9 系统用于敲除 CDH1。

结果

人参皂苷 Rd 抑制 SCC9 细胞的生长并增加其凋亡。人参皂苷 Rd 还抑制 SCC9 细胞的迁移和侵袭。H19 和 miR-675-5p 高表达,而 CDH1 和 E-cadherin 表达水平较低。H19 和 miR-675-5p 促进 SCC9 转移。相反,CDH1 和 E-cadherin 抑制 SCC9 细胞的转移。生物信息学分析表明 miR-675-5p 与 CDH1 相关。人参皂苷 Rd 处理后 H19 和 miR-675-5p 的表达降低,而 CDH1 和 E-cadherin 的表达增加。

结论

人参皂苷 Rd 通过 H19/miR-675-5p/CDH1 轴抑制舌癌细胞的迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/3c29c2c59226/1678-7757-jaos-30-e20220144-gf10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/458dad66d133/1678-7757-jaos-30-e20220144-gf06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/1aac3726f6cb/1678-7757-jaos-30-e20220144-gf07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/251f79dd9085/1678-7757-jaos-30-e20220144-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/ac86529dacfe/1678-7757-jaos-30-e20220144-gf08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/841dca70c2b6/1678-7757-jaos-30-e20220144-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/880e73fe0bb1/1678-7757-jaos-30-e20220144-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/36fe478ef50a/1678-7757-jaos-30-e20220144-gf04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/6d2e7fc687fe/1678-7757-jaos-30-e20220144-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/5bd95348bf51/1678-7757-jaos-30-e20220144-gf09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/3c29c2c59226/1678-7757-jaos-30-e20220144-gf10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/458dad66d133/1678-7757-jaos-30-e20220144-gf06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/1aac3726f6cb/1678-7757-jaos-30-e20220144-gf07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/251f79dd9085/1678-7757-jaos-30-e20220144-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/ac86529dacfe/1678-7757-jaos-30-e20220144-gf08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/841dca70c2b6/1678-7757-jaos-30-e20220144-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/880e73fe0bb1/1678-7757-jaos-30-e20220144-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/36fe478ef50a/1678-7757-jaos-30-e20220144-gf04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/6d2e7fc687fe/1678-7757-jaos-30-e20220144-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/5bd95348bf51/1678-7757-jaos-30-e20220144-gf09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33bf/9444189/3c29c2c59226/1678-7757-jaos-30-e20220144-gf10.jpg

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