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靶向自噬可增强放疗对宫颈癌细胞的抗肿瘤作用。

Targeting autophagy promotes the antitumor effect of radiotherapy on cervical cancer cells.

作者信息

Meng Fanjie, Yan Ying, Zhou Li, Zhao Song, Sun Lingyan, Yu Huiying

机构信息

Basic Medical Laboratory, General Hospital of Northern Theater Command, Shenyang, China.

Country Department of Radiotherapy, General Hospital of Northern Theater Command, Shenyang, China.

出版信息

Cancer Biol Ther. 2024 Dec 31;25(1):2431136. doi: 10.1080/15384047.2024.2431136. Epub 2024 Dec 5.

Abstract

Radiotherapy is the mainstay of cancer treatment, and reducing radioresistance is still a poorly explored issue in radiotherapy. Our study was designed to explore the possible functions and mechanisms of autophagy in cervical cancer cells treated with radiotherapy. We discovered that autophagy was activated in C33a and HeLa cervical cancer cells in parallel with increased apoptosis and formation of polyploid giant carcinoma cells (PGCCs) after radiation. Inhibition of autophagy significantly enhances radiation-induced cytotoxicity and apoptosis in cervical cancer cells and reduces PGCCs formation. Immunoblot analysis, as part of the mechanistic experiments, showed that the phosphorylation levels of Akt, mTOR, and P70S6K were downregulated. Thus, our research demonstrated that inhibiting autophagy enhances the antitumor effects of radiation on cervical cancer cells.

摘要

放射疗法是癌症治疗的主要手段,而降低放射抗性在放射治疗中仍是一个研究较少的问题。我们的研究旨在探讨自噬在接受放射治疗的宫颈癌细胞中的可能作用及机制。我们发现,在放射后,C33a和HeLa宫颈癌细胞中的自噬被激活,同时细胞凋亡增加以及多倍体巨癌细胞(PGCCs)形成。抑制自噬可显著增强放射诱导的宫颈癌细胞的细胞毒性和凋亡,并减少PGCCs的形成。作为机制实验的一部分,免疫印迹分析表明,Akt、mTOR和P70S6K的磷酸化水平下调。因此,我们的研究表明,抑制自噬可增强放射对宫颈癌细胞的抗肿瘤作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17f6/11622585/6280614be08b/KCBT_A_2431136_F0001_OC.jpg

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