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MYCL 通过激活 JAK/STAT3 通路促进三阴性乳腺癌的进展。

MYCL promotes the progression of triple‑negative breast cancer by activating the JAK/STAT3 pathway.

机构信息

Department of Breast Surgery, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.

Department of Radiology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.

出版信息

Oncol Rep. 2022 Nov;48(5). doi: 10.3892/or.2022.8418. Epub 2022 Sep 30.

DOI:10.3892/or.2022.8418
PMID:36177900
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9551653/
Abstract

The present study aimed to investigate the underlying regulatory mechanism of MYCL proto‑oncogene (MYCL) in triple‑negative breast cancer (TNBC) progression. experiments were performed to confirm the functional roles of MYCL in TNBC, and its effects on the JAK/STAT3 pathway through flow cytometric analysis, colony formation, wound healing and Transwell assays. In addition, the GSE45498 dataset demonstrated that MYCL was upregulated in TNBC and that it was significantly related to poor survival of patients with TNBC. Knockdown of MYCL induced the apoptosis, and suppressed the proliferation, migration and invasion of TNBC cells by inhibiting the JAK/STAT3 pathway. Notably, MYCL could activate the JAK/STAT3 pathway, whereas inhibition of the JAK/STAT3 pathway could eliminate the effect of MYCL on TNBC cells. Knockdown of MYCL also suppressed the growth of TNBC xenograft tumors. In conclusion, MYCL could promote TNBC progression by activating the JAK/STAT3 pathway.

摘要

本研究旨在探讨 MYCL 原癌基因（MYCL）在三阴性乳腺癌（TNBC）进展中的潜在调控机制。通过流式细胞分析、集落形成、划痕愈合和 Transwell 测定等实验，验证了 MYCL 在 TNBC 中的功能作用及其对 JAK/STAT3 通路的影响。此外，GSE45498 数据集表明，MYCL 在 TNBC 中上调，与 TNBC 患者的不良生存显著相关。敲低 MYCL 可通过抑制 JAK/STAT3 通路诱导 TNBC 细胞凋亡，抑制增殖、迁移和侵袭。值得注意的是，MYCL 可激活 JAK/STAT3 通路，而抑制 JAK/STAT3 通路可消除 MYCL 对 TNBC 细胞的影响。敲低 MYCL 还抑制了 TNBC 异种移植瘤的生长。综上所述，MYCL 可通过激活 JAK/STAT3 通路促进 TNBC 进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/886be9cfe052/or-48-05-08418-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/ffb74ddd5857/or-48-05-08418-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/ada3bd20546e/or-48-05-08418-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/fa6052bc9dac/or-48-05-08418-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/1f3dba19756d/or-48-05-08418-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/64a1874d8318/or-48-05-08418-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/886be9cfe052/or-48-05-08418-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/ffb74ddd5857/or-48-05-08418-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/ada3bd20546e/or-48-05-08418-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/fa6052bc9dac/or-48-05-08418-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/1f3dba19756d/or-48-05-08418-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/64a1874d8318/or-48-05-08418-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c9/9551653/886be9cfe052/or-48-05-08418-g05.jpg

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