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使用TiNIR靶向血红素加氧酶2（HO2），一种治疗转移性非小细胞肺癌的诊疗方法。

Targeting Heme Oxygenase 2 (HO2) with TiNIR, a Theragnostic Approach for Managing Metastatic Non-Small Cell Lung Cancer.

作者信息

Mun Seul-Ki, Sim Hyun Bo, Lee Jae-Hyuk, Kim Hyeongyeong, Park Dae-Han, Lee Yong-An, Han Ji Yeon, Choi Yu-Jeong, Son Jun Sang, Park Jeongwon, Lim Tae-Hwan, Yee Sung-Tae, Chang Young-Tae, Lee Seongsoo, Chang Dong-Jo, Kim Jong-Jin

机构信息

Department of Biomedical Science, Sunchon National University, Suncheon 57922, Republic of Korea.

College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Suncheon 57922, Republic of Korea.

出版信息

Biomater Res. 2024 Apr 25;28:0026. doi: 10.34133/bmr.0026. eCollection 2024.

DOI:10.34133/bmr.0026
PMID:38665698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11045274/
Abstract

Despite notable advancements in cancer therapeutics, metastasis remains a primary obstacle impeding a successful prognosis. Our prior study has identified heme oxygenase 2 (HO2) as a promising therapeutic biomarker for the aggressive subsets within tumor. This study aims to systematically evaluate HO2 as a therapeutic target of cancer, with a specific emphasis on its efficacy in addressing cancer metastasis. Through targeted inhibition of HO2 by TiNIR (tumor-initiating cell probe with near infrared), we observed a marked increase in reactive oxygen species. This, in turn, orchestrated the modulation of AKT and cJUN activation, culminating in a substantial attenuation of both proliferation and migration within a metastatic cancer cell model. Furthermore, in a mouse model, clear inhibition of cancer metastasis was unequivocally demonstrated with an HO2 inhibitor administration. These findings underscore the therapeutic promise of targeting HO2 as a strategic intervention to impede cancer metastasis, enhancing the effectiveness of cancer treatments.

摘要

尽管癌症治疗取得了显著进展，但转移仍然是阻碍预后成功的主要障碍。我们之前的研究已将血红素加氧酶2（HO2）确定为肿瘤侵袭性亚群中有前景的治疗生物标志物。本研究旨在系统评估HO2作为癌症的治疗靶点，特别强调其在解决癌症转移方面的疗效。通过用TiNIR（近红外肿瘤起始细胞探针）靶向抑制HO2，我们观察到活性氧显著增加。这进而精心调控了AKT和cJUN激活的调节，最终在转移性癌细胞模型中使增殖和迁移大幅减弱。此外，在小鼠模型中，给予HO2抑制剂明确显示出对癌症转移的明显抑制作用。这些发现强调了将HO2作为一种战略干预措施靶向治疗以阻止癌症转移、提高癌症治疗效果的治疗前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/61b38ed1b21e/bmr.0026.fig.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/585f96c1b211/bmr.0026.fig.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/00cbb97625bc/bmr.0026.fig.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/2b961e1edf50/bmr.0026.fig.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/016b35a2c78f/bmr.0026.fig.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/543dc8fd4ae7/bmr.0026.fig.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/61b38ed1b21e/bmr.0026.fig.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/585f96c1b211/bmr.0026.fig.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/00cbb97625bc/bmr.0026.fig.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/2b961e1edf50/bmr.0026.fig.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/016b35a2c78f/bmr.0026.fig.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/543dc8fd4ae7/bmr.0026.fig.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93c2/11045274/61b38ed1b21e/bmr.0026.fig.006.jpg

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本文引用的文献

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2
Daidzein Synergizes with Gefitinib to Induce ROS/JNK/c-Jun Activation and Inhibit EGFR-STAT/AKT/ERK Pathways to enhance Lung Adenocarcinoma cells chemosensitivity.染料木黄酮与吉非替尼协同作用诱导 ROS/JNK/c-Jun 激活，抑制 EGFR-STAT/AKT/ERK 通路，增强肺腺癌细胞的化疗敏感性。
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Label-Free Morpho-Molecular Imaging for Studying the Differential Interaction of Black Phosphorus with Tumor Cells.
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Nanomaterials (Basel). 2022 Jun 10;12(12):1994. doi: 10.3390/nano12121994.
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The interferon-β/STAT1 axis drives the collective invasion of skin squamous cell carcinoma with sealed intercellular spaces.干扰素-β/信号转导和转录激活因子1轴驱动具有封闭细胞间隙的皮肤鳞状细胞癌的集体侵袭。
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PI3K/AKT Signaling Tips the Balance of Cytoskeletal Forces for Cancer Progression.PI3K/AKT信号传导影响细胞骨架力平衡以促进癌症进展。
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Targeting PI3K/Akt signal transduction for cancer therapy.针对 PI3K/Akt 信号转导通路的癌症治疗策略。
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Cell cycle control in cancer.癌症中的细胞周期调控。
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