Hsa_circ_0110757 upregulates ITGA1 to facilitate temozolomide resistance in glioma by suppressing hsa-miR-1298-5p.
Hsa_circ_0110757 upregulates ITGA1 to facilitate temozolomide resistance in glioma by suppressing hsa-miR-1298-5p.
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Hsa_circ_0110757通过抑制hsa-miR-1298- 5 p上调ITGA 1以促进胶质瘤中的替莫唑胺耐药性。
DOI：
10.1038/s41419-021-03533-x
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发表时间：
2021-03-05
影响因子：
9
通讯作者：
Zhang C
中科院分区：
文献类型：
--
作者：
Li H;Liu Q;Chen Z;Wu M;Zhang C;Su J;Li Y;Zhang C
替莫唑胺（TMZ）是国际公认的胶质瘤化疗治疗首选药物。然而，神经胶质瘤长期使用后出现TMZ耐药，是一个亟待解决的问题。环状RNA（circRNA）是非编码RNA，在肿瘤的发病机制和进展中发挥重要作用。通过高通量测序分析在 TMZ 抗性神经胶质瘤细胞中鉴定出 Hsa_circ_0110757，该 Hsa_circ_0110757 源自骨髓细胞白血病 1 (Mcl-1) 外显子的反向剪接。在体外和体内评估了 hsa_circ_0110757 在 TMZ 耐药性神经胶质瘤中的作用。结果发现，hsa_circ_0110757 和 ITGA1 在 TMZ 耐药性胶质瘤中比在 TMZ 敏感性胶质瘤中表达更高。接受TMZ治疗的胶质瘤患者中hsa_circ_0110757的过度表达与肿瘤侵袭明显相关。这项研究表明 hsa_circ_0110757 通过海绵 hsa-miR-1298-5p 促进 ITGA1 表达来抑制神经胶质瘤细胞凋亡。因此，hsa_circ_0110757/hsa-miR-1298-5p/ITGA可能是逆转神经胶质瘤对TMZ耐药的潜在治疗靶点。
Temozolomide (TMZ) is the internationally recognized and preferred drug for glioma chemotherapy treatment. However, TMZ resistance in glioma appears after long-term use and is an urgent problem that needs to be solved. Circular RNAs (circRNAs) are noncoding RNAs and play an important role in the pathogenesis and progression of tumors. Hsa_circ_0110757 was identified in TMZ-resistant glioma cells by high-throughput sequencing analysis and was derived from reverse splicing of myeloid cell leukemia-1 (Mcl-1) exons. The role of hsa_circ_0110757 in TMZ-resistant glioma was evaluated both in vitro and in vivo. It was found that hsa_circ_0110757 and ITGA1 are more highly expressed in TMZ-resistant glioma than in TMZ-sensitive glioma. The overexpression of hsa_circ_0110757 in glioma patients treated with TMZ was obviously associated with tumor invasion. This study indicates that hsa_circ_0110757 inhibits glioma cell apoptosis by sponging hsa-miR-1298-5p to promote ITGA1 expression. Thus, hsa_circ_0110757/hsa-miR-1298-5p/ITGA could be a potential therapeutic target for reversing the resistance of glioma to TMZ.
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影响因子：
12.8
作者：
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通讯作者：
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14.5
作者：
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作者：
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