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p38 MAP 激酶在癌症干细胞和转移中的作用。

Role of p38 MAP kinase in cancer stem cells and metastasis.

机构信息

Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Rice University, Houston, TX, 77030, USA.

出版信息

Oncogene. 2022 Jun;41(23):3177-3185. doi: 10.1038/s41388-022-02329-3. Epub 2022 Apr 30.

DOI:10.1038/s41388-022-02329-3
PMID:35501462
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9166676/
Abstract

Therapeutic resistance and metastatic progression are responsible for the majority of cancer mortalities. In particular, the development of resistance is a significant barrier to the efficacy of cancer treatments such as chemotherapy, radiotherapy, targeted therapies, and immunotherapies. Cancer stem cells (CSCs) underlie treatment resistance and metastasis. p38 mitogen-activated protein kinase (p38 MAPK) is downstream of several CSC-specific signaling pathways, and it plays an important role in CSC development and maintenance and contributes to metastasis and chemoresistance. Therefore, the development of therapeutic approaches targeting p38 can sensitize tumors to chemotherapy and prevent metastatic progression.

摘要

治疗抵抗和转移进展是导致大多数癌症死亡的原因。特别是，抵抗的发展是癌症治疗（如化疗、放疗、靶向治疗和免疫治疗）疗效的重大障碍。癌症干细胞（CSC）是治疗抵抗和转移的基础。p38 丝裂原活化蛋白激酶（p38 MAPK）是几种 CSC 特异性信号通路的下游，它在 CSC 的发育和维持中发挥重要作用，并有助于转移和化疗耐药。因此，开发针对 p38 的治疗方法可以使肿瘤对化疗敏感，并防止转移进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/0b4c02a31beb/41388_2022_2329_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/a689831f7161/41388_2022_2329_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/191ce9272cac/41388_2022_2329_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/699d303bf278/41388_2022_2329_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/26fa361160b0/41388_2022_2329_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/0b4c02a31beb/41388_2022_2329_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/a689831f7161/41388_2022_2329_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/191ce9272cac/41388_2022_2329_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/699d303bf278/41388_2022_2329_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/26fa361160b0/41388_2022_2329_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb5/9166676/0b4c02a31beb/41388_2022_2329_Fig5_HTML.jpg

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本文引用的文献

[1]
Compressive stress-mediated p38 activation required for ERα + phenotype in breast cancer.

Nat Commun. 2021-11-29

[2]
Mechanical Stress Signaling in Pancreatic Cancer Cells Triggers p38 MAPK- and JNK-Dependent Cytoskeleton Remodeling and Promotes Cell Migration via Rac1/cdc42/Myosin II.

Mol Cancer Res. 2022-3-1

[3]
AMPK promotes antitumor immunity by downregulating PD-1 in regulatory T cells via the HMGCR/p38 signaling pathway.

Mol Cancer. 2021-10-14

[4]
Survival analysis across the entire transcriptome identifies biomarkers with the highest prognostic power in breast cancer.

Comput Struct Biotechnol J. 2021-7-18

[5]
Survival analysis in breast cancer using proteomic data from four independent datasets.

Sci Rep. 2021-8-18

[6]
p85β alters response to EGFR inhibitor in ovarian cancer through p38 MAPK-mediated regulation of DNA repair.

Neoplasia. 2021-7

[7]
Bone marrow stromal cells induce an ALDH+ stem cell-like phenotype and enhance therapy resistance in AML through a TGF-β-p38-ALDH2 pathway.

PLoS One. 2020

[8]
WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC.

Signal Transduct Target Ther. 2020-4-15

[9]
The Clinical Impact of Cancer Stem Cells.

Oncologist. 2020-2

[10]
Bone secreted factors induce cellular quiescence in prostate cancer cells.

Sci Rep. 2019-12-9

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