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非小细胞肺癌细胞的膜修复能力受耐药性和上皮-间质转化调控。

Membrane Repairing Capability of Non-Small Cell Lung Cancer Cells Is Regulated by Drug Resistance and Epithelial-Mesenchymal-Transition.

作者信息

Xia Xingyu, Yang Hanbo, Au Dennis Wai-Yin, Lai Syrus Pak-Hei, Lin Yuan, Cho William Chi-Shing

机构信息

Department of Mechanical Engineering, The University of Hong Kong, Hong Kong, China.

Department of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong, China.

出版信息

Membranes (Basel). 2022 Apr 15;12(4):428. doi: 10.3390/membranes12040428.

DOI:10.3390/membranes12040428
PMID:35448398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9029135/
Abstract

The plasma membrane separates the interior of the cells from the extracellular fluid and protects the cell from disruptive external factors. Therefore, the self-repairing capability of the membrane is crucial for cells to maintain homeostasis and survive in a hostile environment. Here, we found that micron-sized membrane pores induced by cylindrical atomic force microscope probe puncture resealed significantly (~1.3-1.5 times) faster in drug-resistant non-small cell lung cancer (NSCLC) cell lines than in their drug-sensitive counterparts. Interestingly, we found that such enhanced membrane repairing ability was due to the overexpression of annexin in drug-resistant NSCLC cells. In addition, a further ~50% reduction in membrane resealing time (i.e., from ~23 s to ~13 s) was observed through the epithelial-mesenchymal-transition, highlighting the superior viability and potential of highly aggressive tumor cells using membrane resealing as an indicator for assessing the drug-resistivity and pathological state of cancer.

摘要

质膜将细胞内部与细胞外液分隔开,并保护细胞免受外部干扰因素的影响。因此,膜的自我修复能力对于细胞维持体内平衡并在恶劣环境中生存至关重要。在此,我们发现,圆柱形原子力显微镜探针穿刺诱导的微米级膜孔在耐药性非小细胞肺癌(NSCLC)细胞系中的重新封闭速度明显快得多(约1.3 - 1.5倍),比其对应的药物敏感细胞系更快。有趣的是,我们发现这种增强的膜修复能力是由于耐药性NSCLC细胞中膜联蛋白的过表达所致。此外,通过上皮-间质转化观察到膜重新封闭时间进一步减少了约50%(即从约23秒降至约13秒),突出了使用膜重新封闭作为评估癌症耐药性和病理状态指标的高度侵袭性肿瘤细胞的卓越活力和潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/998e45a361be/membranes-12-00428-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/2c89d05246e5/membranes-12-00428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/4469d315fd07/membranes-12-00428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/c09959b15f21/membranes-12-00428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/c6eefad87018/membranes-12-00428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/998e45a361be/membranes-12-00428-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/2c89d05246e5/membranes-12-00428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/4469d315fd07/membranes-12-00428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/c09959b15f21/membranes-12-00428-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/c6eefad87018/membranes-12-00428-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4798/9029135/998e45a361be/membranes-12-00428-g005.jpg

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Annexin A7 is required for ESCRT III-mediated plasma membrane repair.膜修复需要膜联蛋白 A7 来介导 ESCRT III。
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