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雷尼替胺 T 通过调控 Nrf2 和 STAT3 信号通路抑制黑色素瘤 B16F10 细胞转移和侵袭。

Renieramycin T Inhibits Melanoma B16F10 Cell Metastasis and Invasion via Regulating Nrf2 and STAT3 Signaling Pathways.

机构信息

Department of Pediatric Surgery, Affiliated Hospital of Jining Medical University, Jining 272067, China.

College of Pharmacy, Heze University, Heze 274015, China.

出版信息

Molecules. 2022 Aug 22;27(16):5337. doi: 10.3390/molecules27165337.

DOI:10.3390/molecules27165337
PMID:36014573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9413012/
Abstract

As one of marine tetrahydroisoquinoline alkaloids, renieramycin T plays a significant role in inhibiting tumor metastasis and invasion. However, the effect of renieramycin T on inflammation-related tumor metastasis and invasion is still unknown, and its mechanisms remain unclear. Here we established an inflammation-related tumor model by using the supernatant of RAW264.7 cells to simulate B16F10 mouse melanoma cells. The results indicate that renieramycin T suppressed RAW264.7 cell supernatant-reduced B16F10 cell adhesion to a fibronectin-coated substrate, migration, and invasion through the matrigel in a concentration-dependent manner. Moreover, Western blot results reveal that renieramycin T attenuated the phosphorylation of STAT3 and down-regulated the expression of Nrf2. Together, the above findings suggest a model of renieramycin T in suppressing B16F10 cancer cell migration and invasion. It may serve as a promising drug for the treatment of cancer metastasis.

摘要

作为海洋四氢异喹啉生物碱之一,雷尼替丁 T 在抑制肿瘤转移和侵袭方面发挥着重要作用。然而,雷尼替丁 T 对炎症相关肿瘤转移和侵袭的影响尚不清楚,其机制也尚不清楚。在这里,我们通过使用 RAW264.7 细胞的上清液来模拟 B16F10 小鼠黑色素瘤细胞,建立了一个炎症相关的肿瘤模型。结果表明,雷尼替丁 T 能够浓度依赖性地抑制 RAW264.7 细胞上清液减少的 B16F10 细胞对纤连蛋白包被基底的黏附、迁移和侵袭。此外,Western blot 结果表明,雷尼替丁 T 减弱了 STAT3 的磷酸化,并下调了 Nrf2 的表达。综上所述,这些发现提出了雷尼替丁 T 抑制 B16F10 癌细胞迁移和侵袭的模型。它可能成为治疗癌症转移的一种有前途的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/b849123afb0b/molecules-27-05337-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/09b065a17459/molecules-27-05337-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/9c295b03e3e4/molecules-27-05337-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/c25c29e71d7f/molecules-27-05337-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/0d007ed33719/molecules-27-05337-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/b849123afb0b/molecules-27-05337-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/09b065a17459/molecules-27-05337-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/9c295b03e3e4/molecules-27-05337-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/c25c29e71d7f/molecules-27-05337-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/0d007ed33719/molecules-27-05337-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72a/9413012/b849123afb0b/molecules-27-05337-g005.jpg

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