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hsa_circ_0002874 的过表达通过调节 miR-1273f/MDM2/p53 通路促进非小细胞肺癌对紫杉醇的耐药性。

Overexpression of hsa_circ_0002874 promotes resistance of non-small cell lung cancer to paclitaxel by modulating miR-1273f/MDM2/p53 pathway.

机构信息

Department of Pathology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan 215300, Jiangsu, PR China.

Department of Medical Oncology, Hangzhou Cancer Hospital, Hangzhou 310002, Zhejiang, PR China.

出版信息

Aging (Albany NY). 2021 Feb 17;13(4):5986-6009. doi: 10.18632/aging.202521.

DOI:10.18632/aging.202521
PMID:33612481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7950269/
Abstract

BACKGROUND

This study aimed to investigate the aberrant expression of hsa_circ_0002874 in non-small cell lung cancer (NSCLC) and elucidate associated molecular mechanisms that influence apoptosis and induce paclitaxel (PTX) resistance.

METHODS

Inhibitors were used to downregulate circRNA or miRNA expression. pCDNA plasmid transfection and mimics were used to upregulate circRNA or miRNA expression. Dual-luciferase reporter assays were conducted to evaluate interactions between miR1273f and MDM2. Xenograft tumor models were used to assess the effect of hsa_circ_0002874 and miR1273f on tumor growth. NSCLC tissues and matched non-cancerous tissues were also collected for correlation analysis.

RESULTS

hsa_circ_0002874 acts as a sponge for miR1273f which targets MDM2/P53. The stability of the hsa_circ_0002874/miR1273f/MDM2/P53 pathway was verified by upregulating and downregulating the expression of hsa_circ_0002874 and miR1273f. hsa_circ_0002874 downregulation or miR1273f upregulation reversed the resistance of the A549/Taxol cells in xenograft models. The expression of hsa_circ_0002874 was high, and the level of MDM2 was low in NSCLC tissues. P53 was only weakly expressed in NSCLC tissues with high expression of MDM2.

CONCLUSIONS

hsa_circ_0002874 is strongly expressed in NSCLC tissues and maybe a potential marker for PTX resistance. hsa_circ_0002874 downregulation could regulate miR1273f/MDM2/P53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis and .

摘要

背景

本研究旨在探讨 hsa_circ_0002874 在非小细胞肺癌（NSCLC）中的异常表达及其影响凋亡并诱导紫杉醇（PTX）耐药的相关分子机制。

方法

用抑制剂下调 circRNA 或 miRNA 的表达。用 pCDNA 质粒转染和模拟物上调 circRNA 或 miRNA 的表达。双荧光素酶报告基因实验评估 miR1273f 和 MDM2 之间的相互作用。异种移植肿瘤模型用于评估 hsa_circ_0002874 和 miR1273f 对肿瘤生长的影响。还收集了 NSCLC 组织和匹配的非癌组织进行相关性分析。

结果

hsa_circ_0002874 作为 miR1273f 的海绵，miR1273f 靶向 MDM2/P53。通过上调和下调 hsa_circ_0002874 和 miR1273f 的表达，验证了 hsa_circ_0002874/miR1273f/MDM2/P53 通路的稳定性。hsa_circ_0002874 下调或 miR1273f 上调逆转了异种移植模型中 A549/Taxol 细胞的耐药性。hsa_circ_0002874 在 NSCLC 组织中表达较高，而 MDM2 水平较低。在 MDM2 高表达的 NSCLC 组织中，P53 表达较弱。

结论

hsa_circ_0002874 在 NSCLC 组织中表达较强，可能是 PTX 耐药的潜在标志物。hsa_circ_0002874 下调可调节 miR1273f/MDM2/P53 信号通路，逆转 NSCLC 的 PTX 耐药性并诱导凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/5945b4fd4d74/aging-13-202521-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/c068e5a8484e/aging-13-202521-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/b155a50a08f4/aging-13-202521-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/393ba4638317/aging-13-202521-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/da5fd04a7770/aging-13-202521-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/5945b4fd4d74/aging-13-202521-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/c068e5a8484e/aging-13-202521-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/393ba4638317/aging-13-202521-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/da5fd04a7770/aging-13-202521-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dae/7950269/5945b4fd4d74/aging-13-202521-g008.jpg

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