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癌细胞通过富含 miR-let-7c 的小细胞外囊泡介导的 p53/PTEN 下调来使正常上皮细胞发生恶变。

Cancer cells corrupt normal epithelial cells through miR-let-7c-rich small extracellular vesicle-mediated downregulation of p53/PTEN.

机构信息

The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory for Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.

Shenzhen PKU-HKUST Medical Center (Peking University Shenzhen Hospital), Shenzhen, China.

出版信息

Int J Oral Sci. 2022 Jul 19;14(1):36. doi: 10.1038/s41368-022-00192-2.

DOI:10.1038/s41368-022-00192-2
PMID:35851058
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9293927/
Abstract

Tumor volume increases continuously in the advanced stage, and aside from the self-renewal of tumor cells, whether the oncogenic transformation of surrounding normal cells is involved in this process is currently unclear. Here, we show that oral squamous cell carcinoma (OSCC)-derived small extracellular vesicles (sEVs) promote the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of normal epithelial cells but delay their apoptosis. In addition, nuclear-cytoplasmic invaginations and multiple nucleoli are observed in sEV-treated normal cells, both of which are typical characteristics of premalignant lesions of OSCC. Mechanistically, miR-let-7c in OSCC-derived sEVs is transferred to normal epithelial cells, leading to the transcriptional inhibition of p53 and inactivation of the p53/PTEN pathway. In summary, we demonstrate that OSCC-derived sEVs promote the precancerous transformation of normal epithelial cells, in which the miR-let-7c/p53/PTEN pathway plays an important role. Our findings reveal that cancer cells can corrupt normal epithelial cells through sEVs, which provides new insight into the progression of OSCC.

摘要

肿瘤体积在晚期持续增加，除了肿瘤细胞的自我更新外，周围正常细胞的致癌转化是否参与这一过程目前尚不清楚。在这里，我们表明口腔鳞状细胞癌 (OSCC) 衍生的小细胞外囊泡 (sEVs) 促进正常上皮细胞的增殖、迁移、侵袭和上皮-间充质转化 (EMT)，但会延迟它们的凋亡。此外，sEV 处理的正常细胞中观察到核质内陷和多个核仁，这两者都是 OSCC 癌前病变的典型特征。在机制上，OSCC 衍生的 sEV 中的 miR-let-7c 被转移到正常上皮细胞中，导致 p53 的转录抑制和 p53/PTEN 通路失活。总之，我们证明 OSCC 衍生的 sEV 促进了正常上皮细胞的癌前转化，其中 miR-let-7c/p53/PTEN 通路发挥着重要作用。我们的发现表明，癌细胞可以通过 sEV 使正常上皮细胞发生恶变，这为 OSCC 的进展提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/fbb208264cc6/41368_2022_192_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/10a976f3d255/41368_2022_192_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/318c20c6b772/41368_2022_192_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/152983230eb1/41368_2022_192_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/0d4ed5d93c01/41368_2022_192_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/206bfee1ac9a/41368_2022_192_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/fbb208264cc6/41368_2022_192_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/10a976f3d255/41368_2022_192_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/318c20c6b772/41368_2022_192_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/152983230eb1/41368_2022_192_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/0d4ed5d93c01/41368_2022_192_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/206bfee1ac9a/41368_2022_192_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7194/9293927/fbb208264cc6/41368_2022_192_Fig6_HTML.jpg

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