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SNHG16 promotes osteosarcoma progression and enhances cisplatin resistance by sponging miR-16 to upregulate ATG4B expression.SNHG16 通过海绵吸附 miR-16 促进骨肉瘤的进展并增强顺铂耐药性，从而上调 ATG4B 的表达。
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Theranostic Nanoprobe Mediated Simultaneous Monitoring and Inhibition of P-Glycoprotein Potentiating Multidrug-Resistant Cancer Therapy.治疗诊断纳米探针介导的同时监测和抑制 P-糖蛋白增强多药耐药性癌症治疗。
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Intracellular Doppler Spectroscopy detects altered drug response in SKOV3 tumor spheroids with silenced or inhibited P-glycoprotein.细胞内多普勒光谱检测沉默或抑制 P-糖蛋白的 SKOV3 肿瘤球体中药物反应的改变。
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P-Glycoprotein Overexpression Is Associated With Cisplatin Resistance in Human Osteosarcoma.P-糖蛋白过表达与人骨肉瘤顺铂耐药相关。
Anticancer Res. 2019 Apr;39(4):1711-1718. doi: 10.21873/anticanres.13277.
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Apoptin-derived peptide reverses cisplatin resistance in gastric cancer through the PI3K-AKT signaling pathway.凋亡素衍生肽通过 PI3K-AKT 信号通路逆转胃癌对顺铂的耐药性。
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Exosomal delivery of berry anthocyanidins for the management of ovarian cancer.外泌体递送浆果花色苷用于卵巢癌的管理。
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miR-491 Inhibits Osteosarcoma Lung Metastasis and Chemoresistance by Targeting αB-crystallin.miR-491 通过靶向 αB-晶状体蛋白抑制骨肉瘤肺转移和化疗耐药性。
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Baicalein increases cisplatin sensitivity of A549 lung adenocarcinoma cells via PI3K/Akt/NF-κB pathway.黄芩素通过 PI3K/Akt/NF-κB 通路增加 A549 肺腺癌细胞对顺铂的敏感性。
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Location of residual viable tumor cells after neoadjuvant chemotherapy: A new concept with high prognostic performance in osteosarcoma.新辅助化疗后残留存活肿瘤细胞的位置：骨肉瘤中具有高预后性能的新概念。
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MARK2通过PI3K/AKT/NF-κB信号通路增强骨肉瘤细胞对顺铂的耐药性。

MARK2 enhances cisplatin resistance via PI3K/AKT/NF-κB signaling pathway in osteosarcoma cells.

作者信息

Wei Xianfu, Xu Liang, Jeddo Salim Fa, Li Ka, Li Xin, Li Jianmin

机构信息

Department of Orthopedics, Qilu Hospital, Shandong University Jinan 250012, Shandong, China.

Department of Orthopedics, Affiliated Hospital of Shandong Academy of Medical Sciences Jinan 250031, Shandong, China.

出版信息

Am J Transl Res. 2020 May 15;12(5):1807-1823. eCollection 2020.

PMID:32509178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7270034/
Abstract

Osteosarcoma is the most common primary bone malignancy found in children and young adults. Chemotherapy resistance, especially to cisplatin, presents a major clinical challenge in the treatment and prognosis of osteosarcoma. New biomarkers and mechanisms of cisplatin resistance in osteosarcoma are urgently needed due to poor survival outcomes and currently inadequate treatments. In this study, we investigate the role and potential mechanisms of microtubule-affinity regulating kinase2 (MARK2) during osteosarcoma cisplatin resistance. Gene Expression Omnibus dataset analyses indicated that high MARK2 expression was associated with poor prognosis and may positively correlate with chemoresistance. Moreover, we showed that MARK2 was significantly upregulated in osteosarcoma cells compared with normal cells. The overexpression and inhibition of MARK2 promoted and suppressed, respectively, cisplatin resistance in osteosarcoma cells and . Mechanistically, MARK2 overexpression enhanced P-glycoprotein expression and decreased cell apoptosis through PI3K/AKT/NF-κB signaling pathway activation, resulting in cisplatin resistance. Our results suggest that high MARK2 expression can enhance cisplatin resistance in osteosarcoma cells, supporting the potential of MARK2 as a new therapeutic target and biomarker for predicting cisplatin resistance in osteosarcoma.

摘要

骨肉瘤是儿童和年轻成人中最常见的原发性骨恶性肿瘤。化疗耐药，尤其是对顺铂的耐药，是骨肉瘤治疗和预后的主要临床挑战。由于生存结果不佳且目前治疗方法不足，迫切需要骨肉瘤中顺铂耐药的新生物标志物和机制。在本研究中，我们探究了微管亲和力调节激酶2（MARK2）在骨肉瘤顺铂耐药过程中的作用及潜在机制。基因表达综合数据库分析表明，高MARK2表达与预后不良相关，且可能与化疗耐药呈正相关。此外，我们发现与正常细胞相比，骨肉瘤细胞中MARK2显著上调。MARK2的过表达和抑制分别促进和抑制了骨肉瘤细胞的顺铂耐药。机制上，MARK2过表达通过激活PI3K/AKT/NF-κB信号通路增强P-糖蛋白表达并减少细胞凋亡，从而导致顺铂耐药。我们的结果表明，高MARK2表达可增强骨肉瘤细胞的顺铂耐药性，支持MARK2作为预测骨肉瘤顺铂耐药的新治疗靶点和生物标志物的潜力。