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ABCB5通过促炎细胞因子信号传导回路维持黑色素瘤起始细胞。

ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.

作者信息

Wilson Brian J, Saab Karim R, Ma Jie, Schatton Tobias, Pütz Pablo, Zhan Qian, Murphy George F, Gasser Martin, Waaga-Gasser Ana Maria, Frank Natasha Y, Frank Markus H

机构信息

Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Transplant Research Program, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Department of Medicine, VA Boston Healthcare System, Boston, Massachusetts.

Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Transplant Research Program, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.

出版信息

Cancer Res. 2014 Aug 1;74(15):4196-207. doi: 10.1158/0008-5472.CAN-14-0582. Epub 2014 Jun 16.

DOI:10.1158/0008-5472.CAN-14-0582
PMID:24934811
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4119553/
Abstract

The drug efflux transporter ABCB5 identifies cancer stem-like cells (CSC) in diverse human malignancies, where its expression is associated with clinical disease progression and tumor recurrence. ABCB5 confers therapeutic resistance, but other functions in tumorigenesis independent of drug efflux have not been described that might help explain why it is so broadly overexpressed in human cancer. Here we show that in melanoma-initiating cells, ABCB5 controls IL1β secretion, which serves to maintain slow cycling, chemoresistant cells through an IL1β/IL8/CXCR1 cytokine signaling circuit. This CSC maintenance circuit involved reciprocal paracrine interactions with ABCB5-negative cancer cell populations. ABCB5 blockade induced cellular differentiation, reversed resistance to multiple chemotherapeutic agents, and impaired tumor growth in vivo. Together, our results defined a novel function for ABCB5 in CSC maintenance and tumor growth.

摘要

药物外排转运体ABCB5可识别多种人类恶性肿瘤中的癌症干细胞样细胞（CSC），其表达与临床疾病进展和肿瘤复发相关。ABCB5赋予治疗抗性，但尚未描述其在肿瘤发生中独立于药物外排的其他功能，而这些功能可能有助于解释它为何在人类癌症中如此广泛地过度表达。在此我们表明，在黑色素瘤起始细胞中，ABCB5控制IL1β的分泌，IL1β通过IL1β/IL8/CXCR1细胞因子信号传导回路维持缓慢循环、化学抗性细胞。这种CSC维持回路涉及与ABCB5阴性癌细胞群体的相互旁分泌相互作用。ABCB5阻断诱导细胞分化，逆转对多种化疗药物的抗性，并在体内损害肿瘤生长。总之，我们的结果确定了ABCB5在CSC维持和肿瘤生长中的新功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/2e2965b5c64d/nihms604207f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/a162e8d18813/nihms604207f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/e125eb0de758/nihms604207f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/0b49bc8e301c/nihms604207f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/bfe6c424cb89/nihms604207f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/2e2965b5c64d/nihms604207f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/a162e8d18813/nihms604207f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/e125eb0de758/nihms604207f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/0b49bc8e301c/nihms604207f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/bfe6c424cb89/nihms604207f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2010/4119553/2e2965b5c64d/nihms604207f5.jpg

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Testing the cancer stem cell hypothesis in melanoma: the clinics will tell.在黑色素瘤中检验癌症干细胞假说：临床将给出答案。
Pigment Cell Melanoma Res. 2025 Jul;38(4):e70011. doi: 10.1111/pcmr.70011.
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Inter-Relationship Between Melanoma Vemurafenib Tolerance Thresholds and Metabolic Pathway Choice.黑色素瘤维莫非尼耐受阈值与代谢途径选择之间的相互关系。
Cells. 2025 Jun 18;14(12):923. doi: 10.3390/cells14120923.
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Integrated pan-cancer analysis revealed therapeutic targets in the ABC transporter protein family.整合性泛癌分析揭示了ABC转运蛋白家族中的治疗靶点。
PLoS One. 2025 May 30;20(5):e0308585. doi: 10.1371/journal.pone.0308585. eCollection 2025.
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Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.解析缺氧、癌细胞干性和耐药性三者之间的关系。
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