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钙网织蛋白表达控制细胞氧化还原、干性和放射敏感性，可作为神经母细胞瘤放疗的新型辅助剂。

Calreticulin Expression Controls Cellular Redox, Stemness, and Radiosensitivity to Function as a Novel Adjuvant for Radiotherapy in Neuroblastoma.

机构信息

Department of Pathology and Laboratory Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.

School of Medicine, Chung Shan Medical University, Taichung, Taiwan.

出版信息

Oxid Med Cell Longev. 2023 Jan 6;2023:8753309. doi: 10.1155/2023/8753309. eCollection 2023.

DOI:10.1155/2023/8753309
PMID:36644580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9839411/
Abstract

Radiotherapy (RT) is currently only used in children with high-risk neuroblastoma (NB) due to concerns of long-term side effects as well as lack of effective adjuvant. Calreticulin (CALR) has served distinct physiological roles in cancer malignancies; nonetheless, impact of radiation on chaperones and molecular roles they play remains largely unknown. In present study, we systemically analyzed correlation between CALR and NB cells of different malignancies to investigate potential role of CALR in mediating radioresistance of NB. Our data revealed that more malignant NB cells are correlated to lower CALR expression, greater radioresistance, and elevated stemness as indicated by colony- and neurospheroid-forming abilities and vice versa. Of note, manipulating CALR expression in NB cells of varying endogenous CALR expression manifested changes in not only stemness but also radioresistant properties of those NB cells. Further, CALR overexpression resulted in greatly enhanced ROS and led to increased secretion of proinflammatory cytokines. Importantly, growth of NB tumors was significantly hampered by CALR overexpression and was synergistically ablated when RT was also administered. Collectively, our current study unraveled a new notion of utilizing CALR expression in malignant NB to diminish cancer stemness and mitigate radioresistance to achieve favorable therapeutic outcome for NB.

摘要

放射治疗（RT）目前仅用于高危神经母细胞瘤（NB）儿童，因为担心长期副作用以及缺乏有效的辅助治疗。钙网蛋白（CALR）在癌症恶性肿瘤中具有明显的生理作用；然而，辐射对伴侣蛋白的影响及其所发挥的分子作用在很大程度上仍不清楚。在本研究中，我们系统地分析了 CALR 与不同恶性肿瘤的 NB 细胞之间的相关性，以研究 CALR 在介导 NB 放射抵抗中的潜在作用。我们的数据表明，恶性程度更高的 NB 细胞与 CALR 表达水平较低、放射抵抗能力更强以及干细胞特性更高相关，反之亦然。值得注意的是，在具有不同内源性 CALR 表达的 NB 细胞中操纵 CALR 表达不仅改变了干细胞特性，而且改变了这些 NB 细胞的放射抵抗特性。此外，CALR 过表达导致 ROS 大量增加，并导致促炎细胞因子的分泌增加。重要的是，CALR 过表达显著抑制了 NB 肿瘤的生长，并与放射治疗协同抑制了肿瘤的生长。综上所述，我们的研究揭示了利用 CALR 在恶性 NB 中的表达来减少癌症干细胞特性和减轻放射抵抗以实现 NB 有利治疗结果的新观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/7cc6aea07be5/OMCL2023-8753309.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/6c285ca253c2/OMCL2023-8753309.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/b122ec5e8839/OMCL2023-8753309.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/bdfa42ab8f87/OMCL2023-8753309.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/b4cc6d2728f8/OMCL2023-8753309.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/577f97108e2e/OMCL2023-8753309.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/7cc6aea07be5/OMCL2023-8753309.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/6c285ca253c2/OMCL2023-8753309.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/b122ec5e8839/OMCL2023-8753309.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/bdfa42ab8f87/OMCL2023-8753309.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/13c95c3599ad/OMCL2023-8753309.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/b4cc6d2728f8/OMCL2023-8753309.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/577f97108e2e/OMCL2023-8753309.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5990/9839411/7cc6aea07be5/OMCL2023-8753309.007.jpg

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